CVS exam 2
Acute pericarditis
(must meet 2/4 criteria): pericarditic chest pain (sharp, worse with laying flat than sitting up), PERICARDIAL RUB, NEW WIDESPREAD ST-ELEVATION or PR DEPRESSION, and new/worsening PERICARDIAL EFFUSION.
Right axis deviation
+90 to 180 degrees. In this range, the electrical forces of the heart have shifted to the right. This can result from emphysema, left sided MI, right ventricular hypertrophy, pulmonary hypertension, pulmonary embolism.
Normal axis
-30 to +90 degrees. In this range, the electrical forces of the heart are moving in the normal direction.
Left axis deviation
-30 to -90 degrees. In this range, the electrical forces of the heart are shifted to the left. This can result from aortic stenosis, obesity, LBBB, LV dilation, or LV hypertrophy.
Normal PR interval
0.12-0.2 seconds (3-5 small boxes). Goes from the beginning of the P wave to the beginning of the QRS complex, and it represents the time it takes for action potentials to travel from the SA node through the AV node
Height of EKG paper
1 small box=1 mm=0.1 mV. 2 large boxes=1mV
Left ventricular volume curve
1) Atrial systole (LV volume is increasing due to contraction of LA, then mitral valve closes). 2) Isovolumetric ventricular contraction (mitral valve has just closed and aortic valve is not yet open, so volume is constant, known as the LV EDV. Aortic valve opens at end of phase 2). 3) Rapid ventricular ejection (LV volume significantly decreases). 4) Slower ventricular ejection (LV volume continues to decrease). 5) Isovolumentric ventricular relaxation (aortic valve closes and LV relaxes while volume remains constant, known as LV ESV. at the end of this phase, the mitral valve opens). 6) Rapid ventricular filling (after mitral valve opens, filling of ventricle occurs and LV volume increases). 7) slower ventricular filling (LV volume continues to decrease. this phase is also called DIASTASIS).
Electrocardiogram curve
1) Atrial systole (P wave, associated with atrial depolarization, and PR interval). 2) Isovolumetric ventricular contraction (QRS occurs here. R wave reaches its peak just before phase 2, and repolarization also begins). 3) Rapid ventricular ejection (ST segment. 4) Slower ventricular ejection (T wave). 5) Isovolumentric ventricular relaxation (ventricle remains relaxed during diastole, so this is the TP segment). 6) rapid ventricular filling (TP segment). 7) slower ventricular filling (TP segment).
Aortic pressure curve
1) Atrial systole (aortic pressure is gradually declining as blood moves through the atria into systemic vessels). 2) Isovolumetric ventricular contraction (aortic pressure continues to decline while LV pressure is increasing, and when LV pressure>aortic pressure, the aortic valve opens). 3) Rapid ventricular ejection (aortic pressure increases rapidly as blood is ejected into the aorta). 4) Slower ventricular ejection (aortic pressure continues to increase as final 1/3 of blood is ejected into aorta. when aortic pressure>LV pressure, aortic valve closes). 5) Isovolumentric ventricular relaxation (slight rise in aortic pressure called the DICROTIC NOTCH due to closure of the aortic valve). 6) rapid ventricular filling (aortic pressure gradually decreases). 7) slower ventricular filling (same as phase 6).
Left ventricular pressure curve
1) Atrial systole (atrial contraction, which causes the mitral valve to close and LV pressure increases slightly). 2) isovolumetric ventricular contraction (pressure in ventricle begins to increase to generate enough pressure to open the aortic valve). 3) Rapid ventricular ejection (LV pressure exceeds aortic pressure, causing opening of aortic valve and blood is ejected into aorta). 4) Slower ventricular ejection (remain 1/3 of blood is ejected into aorta. when aorta pressure>LV pressure, aortic valve closes). 5) Isovolumetric ventricular relaxation (decrease in LV pressure due to muscle relaxing. when LA pressure>LV pressure, the mitral valve opens). 6) Rapid ventricular filling (rapid passive filling of LV while ventricle is relaxed). 7) Slower ventricular filling (same as 6 but occurs slower).
Phonocardiogram curve
1) Atrial systole. 2) Isovolumetric ventricular contraction (S1 heart sound occurs, associated with closure of AV valves). 3) Rapid ventricular ejection. 4) Slower ventricular ejection. 5) Isovolumentric ventricular relaxation (S2 heart sound, caused by the closure of the semilunar valves). 6) rapid ventricular filling. 7) slower ventricular filling.
Heart valves from largest to smallest (cross-sectional area)
1) tricuspid. 2) mitral. 3) pulmonic. 4) aortic.
Speed of EKG paper
25 mm/sec. 1 small box=1 mm=40 ms=0.04s. 1 big box=200 ms=.2 s. 5 large boxes=1 second
Dairy fat and risk of cardiovascular disease
3 cohort studies showed that there is no significant reduction in risk of CVD when subjects consumed equivalent amount of carbohydrates and dairy fat. However, there is a 24% decreased risk of developing CVD when subjects replaced 5% of energy intake from dairy fat with equivalent amount of polyunsaturated fatty acid or vegetable fat. The 3rd cohort study shows that when subjects substituted 5% energy intake of dairy fait with other animal fat (red meat), there is 6% increased CVD risk.
Mitral valve prolapse
3% with mitral valve prolapse develop one of the 4 serious complications: infective endocarditis, mitral insufficiency w/ or w/o chordal rupture, stroke or systemic infarct (due to embolism of leaflet thrombi), or arrhythmias (both ventricular or atrial). Gross findings: Hooding of the mitral leaflet, which is thickened, enlarged, redundant, and rubbery. Tendinous cords are elongated and thinned (may also involve the tricuspid, aortic, or pulmonary valves). Histology: marked THICKENING OF THE SPONGIOSA LAYER, deposition of MUCOID "MYXOMATOUS" MATERIAL. Causes: most cases have unknown cause. Can be due to Marfan syndrome (defects in FBN-1 ALTER CELL-MATRIX INTERACTIONS AND DYSREGULATE TGF-β SIGNALING), and there are AUTOSOMAL DOMINANT FORMS OF MVP that have been mapped to other genetic loci.
Biventricular pacemaker aka Cardiac resynchronization therapy (CRT)
30% of patients with systolic HF also have evidence of VENTRICULAR DYSYNCHRONY (evidenced by QRS >130 ms, often a LBBB) caused by abnormalities in the electrical depolarization of the ventricle. If a patient has impairment of contractile function and also has electrical dysynchrony, then there is even worse ventricular function, resulting in limited exercise tolerance, impaired quality of life and functional capacity, and poor LV systolic function. A biventricular pacemaker attempts to depolarize the R and L ventricles at the same time, and resynchronize septal depolarization with the rest of the LV. Now the septum and lateral wall contract at the same time. It has been shown to be effective in patients who have EJECTION FRACTION <35% AT BASELINE: it improves long term outcomes, survival, and functional capacity. CRT has been shown to improve mortality & hospitalization rates, functional capacity, and exercise capacity
QRS interval
<0.12 seconds (less than 3 small boxes). Goes from the beginning to the end of the QRS, and represents the time it takes for ventricular depolarization.
QT interval
<0.42 seconds. Goes from the beginning of the QRS complex to the end of the T wave and represents the time between initiation of the QRS complex and the end of the T wave (time for depolarization and repolarization)
TAVR: transcutaneous aortic valve replacement
A collapsed valve is threaded through a catheter and put into the aortic position, and opens up the aortic valve.
Waterhammer pulse
A physical sign of aortic regurgitation. The pulse elevation accentuates the steep rise-and-fall character of the pulse, which seems to slap harder and faster against the fingers. When elevated, the pulse is not sustained (it is more of a tap).
Muller's sign
A physical sign of aortic regurgitation. There is pulsation of the uvula.
Traube's sign
A physical sign of aortic regurgitation. a "pistol-shot" sound heard over femoral pulse
Quincke's sign
A physical sign of aortic regurgitation. capillary pulsation in the nail bed that is visible on applying gentle pressure to induce a degree of whitening.
Duroziez's sign
A physical sign of aortic regurgitation. caused by retrograde diastolic flow in the femoral artery. When stethoscope is placed on the femoral pulses to occlude the artery distally, you can hear turbulent flow in a "to and fro" murmur
De Musset's sign
A physical sign of aortic regurgitation. nodding of the head in time with the heartbeat
Corrigan's sign
A physical sign of aortic regurgitation. visible arterial pulsation in the neck (from flow moving in and out rapidly).
Junctional rhythm
A>V (more atrial events than ventricular events)
Heart failure: pharmacologic treatment
ACE inhibitors or ARBs. Beta blockers. Endopeptidase inhibitors (very new). Spironolactone. Hydralazine+Nitrates (approved for african americans on top of standard therapy). Diuretics (for symptomatic relief/congestion). Digoxin (can relieve some symptoms but does not improve long-term outcomes in patients with HF).
Parasympathetic effect on HR
ACh is released from parasympathetic neurons → activates muscarinic receptors of autorhythmic cells → INCREASES POTASSIUM EFFLUX AND DECREASES CALCIUM INFLUX → hyperpolarization of cell membrane and decreased rate of depolarization → decreased HR.
Purkinje fibers
AP firing rate is 20-40 APs/min. A person could not survive with the Purkinje fibers as the pacemaker. They would require an external pacemaker.
AV node
AP firing rate is 40-60 APs/min. The AV node can be the normal pacemaker if the rate is ~60 BPM. If lower, the person would need a pacemaker.
Decreased oxygen supply at cellular level
ATP DEPLETION → ion pump dysfunction → cellular edema → hydrolysis of cellular membranes/cellular death.
PE: pathophysiology of RV dysfunction.
Acute PE → lungs get acutely hypoxic → hypoxia causes VASOCONSTRICTION of the lungs → pulmonary vascular resistance increases very high → causes worsened RV pressure overload. As RV becomes weak (HYPOKINETIC) it dilates → cardiac output from RV decreases → interventricular septum bows into the LV, which further impedes the LV from filling → cardiac output drops. In addition, as RV becomes pressure overloaded → RV wall tension increases → increased RV myocardial oxygen demand → RV ischemia and/or infarction can occur → further leads to hypokinesis of RV and dilation → decreased RV myocardial oxygen supply → decreased coronary artery perfusion → systemic arterial hypotension. This can lead to HYPOTENSION, SHOCK, AND DEATH. In severe cases, patients have 50-60% mortality.
Orthodromic AV reciprocating tachycardia
An AV nodal dependent tachycardia in which there is conduction from A→V through AV node and V→A (slow) through the accessory pathway. EKG shows NARROW QRS.
Antidromic AV nodal reciprocating tachycardia
An AV nodal dependent tachycardia in which there is conduction from A→V via the accessory pathway and then conduction from V→A via the AV nodal pathway. Because the conduction does not go through the normal AV node→bundle system, the EKG shows WIDE COMPLEX QRS.
Acute pericarditis: treatment
Anti-inflammatory medications are the mainstay treatment: First line: Aspirin (750-1000 mg every 8 hours for 1-2 weeks) or Ibuprofen (600 mg every 8 hours for 1-2 weeks) AND COLCHICINE (0.5 mg for 3 MONTHS). Important: EXERCISE RESTRICTION (because exercising can provoke ventricular arrhythmias). Second line: low-dose corticosteroids (after you have already ruled out bacterial/infectious cause)
Pulmonary arterial hypertension (group 1 PA): treatment algorithm
Anticoagulation + Diuretic + oxygen + Digoxin (to help RV function). Some people get treated with CCBs, and lower risk patients get treated with pulmonary vasodilators (endothelin receptor antagonists or phosphodiesterase type 5 inhibitors). Higher risk patients get treated with Prostacyclins (IV or inhaled) that cause increased production of NO within the lung. In end-stage cases, atrial septostomy (putting a hole in the RA septum to connect it to the LA, which brings more pressure to the left side but circulates deoxygenated blood) or lung transplant.
PV loop of the pericardium
As the volume of the pericardial fluid increases, pressure increases very rapidly. If pericardial pressure > RA pressure, then the pericardial pressure collapses the right side of the heart (which is at less pressure). If the right side of the heart is collapsed, then the volume going into the left side of the heart is decreased, so cardiac output overall is decreased and blood pressure drops. Note: If there is slow accumulation of pericardial fluid (due to a chronic condition such as renal failure), the pericardium can stretch and accommodate fluid for a longer time than if there is an acute insult (such as stab wound). Acute pericardial effusion causes tamponade much faster than chronic pericardial effusion.
Changes in flow during exercise
At rest, organs that get more circulation: digestive tract, liver, kidneys, skeletal muscle. During exercise, skeletal muscle circulation increases by 1066%, heart flow increases 367%, and skin flow also increases 370%. GI tract, kidneys, and bones get decreased flow. Despite decrease in flow to certain tissues, their ability to EXTRACT OXYGEN IS INCREASED from baseline. Tissues that extract high amounts of oxygen at rest (brain and coronary circulation) are dependent on INCREASED FLOW during exercise to achieve adequate oxygenation.
Vasodilating & natriuretic hormones (good)
Atrial natriuretic factor, NO, and prostaglandins.
Atrial fibrillation with uncontrolled conduction to the ventricle
Atrium is in atrial fibrillation. The AV node is decrimental so it blocks some of the signals, but the accessory pathway is not decrimental. Signals from the AV node are unopposed via the accessory pathway, which leads to a ventricular HR of ~400 BPM. This leads to ventricular fibrillation and sudden death. It is VERY dangerous and can lead to sudden cardiac death in young kids. EKG shows irregularly irregular pattern and wide complex tachycardia. Treatment: if unstable, electrical cardioversion. If stable, IV PROCAINAMIDE (1A agent). Do not use AV nodal blocking agents (beta blockers or calcium channel blockers). Do not use Amiodarone. Again: This should NOT BE TREATED WITH AV NODAL BLOCKING AGENTS.
Nutrient-drug interactions: Hydrochlorothiazide
B2, potassium, magnesium, and zinc depleting
AHA's diet recommendations
Balanced diet. Balance calorie intake and physical activity to maintain healthy body weight. Consume whole-grain, high-fiber foods (35 g/day for men, 25 g/day for women). Consume fish, especially oily fish at least twice per week. Minimize intake of beverages and foods with added sugar. Choose and prepare foods with little or no salt. Alcohol consumption in moderation. Limit intake of saturated fat to <7% and trans fat to <1% (or not at all). Minimize intake of partially hydrogenated fats.
Prophylaxis for endocarditis
Before any dental work, patients with certain conditions should get antibiotics 1 hour prior to the dental work. These groups include patients with PROSTHETIC HEART VALVES, previous infective endocarditis, CARDIAC TRANSPLANT RECIPIENTS WITH VALVE REGURGITATION due to a structurally abnormal valve, or certain patients with congenital heart disease. Most common prophylaxis drug is Amoxicillin.
Primary pericardial masses
Benign: fibroma and lipoma. Malignant: Mesotheloma, angiosarcoma, & fibrosarcoma. ALL ARE RARE.
Long term treatment/prevention of arrhythmias
Beta blockers (maximize dose as much as patient can tolerate), Amiodarone (just deal with the side effects), Sotalol (class 3), or Mexilitine (class 1B, given VERY rarely)
Things that cause wide QRS on EKG
Bundle branch blocks, paced beats, accessory pathway (A→V conduction is through the accessory pathway), and beats that originate in the ventricular (ventricular tachycardia)
Heart failure: clinical findings
Can appear well at rest in early heart failure, but can appear cachectic (pale, weight loss) and dusky-colored with advanced disease. Pulmonary exam shows RALES (due to fluid), wheezes, rhonchi, pleural effusions, Cheyne-Stokes respirations (rapid deep breathing followed by shallow breathing/apnea). Increased jugular venous pressure. Hepatomegaly and hepatojugular reflux. Peripheral edema. Cardiac findings: CARDIOMEGALY, S3 GALLOP mitral/tricuspid regurgitation (because the heart is distended and the annulus of the valve are pulled apart), PULSUS ALTERNANS (variation in intensity of pulse from beat to beat)
Cardiac function curve and vascular function curve
Cardiac function curve: demonstrates the direct relationship between central venous pressure (RA pressure) on cardiac output (Frank-Starling Law). Venous return curve aka Vascular function curve: demonstrates the inverse effect of central venous pressure on venous return. The intersection point is known as the EQUILIBRIUM / STEADY STATE (where cardiac output=venous return). The equilibrium point normally occurs when RA pressure=2 mmHg and venous return=5 L/min. If the curves are shifted, the equilibrium point is also shifted.
Changes that occur during exercise
Cardiac output increases (due to parasympathetic withdrawl) and stroke volume increases due to increased venous return (due to both venoconstriction and skeletal muscle compression). Sympathetic system gets activated to increase cardiac output, catecholamine levels, distribution of blood flow, and body temperature.
Physiologic receptors at carotid bodies
Carotid bodies sense decreased pressure/volume and get activated. They are also activated by hypoxia, hypercapnea, acidosis (if pH is below 7.4, such as by lactic acid buildup). When activated, these receptors send signals through carotid sinus nerve to respiratory centers. If respiratory center gets activated, rate of respiration is increased, and O2 level in the body increases. If respiratory center does not get activated, HR is slowed down (by vagus activation), coronary vasodilation, increased systemic vascular resistance.
Changes in venous resistance
Central venous pressure=right atrial pressure. Normal right atrial pressure is ~2-5 mmHg. Normal peripheral venous compartment pressure is ~7 mmHg. This pressure gradient is responsible for venous return. Increasing peripheral venous pressure while keeping the central venous pressure the same would lead to increased venous return. Increasing central venous pressure while keeping the peripheral venous pressure reduces the venous return. Venous resistance (constriction of the venous vessels) reduces venous capacitance and affects blood volume that is coming back into the central venous compartment.
Beta blockers
Class 2 AADs. They block the beta receptors. They mostly target the SA and AV nodal action potential by decreasing the phase 4 slope (and decreasing rate of SA node) and decreasing the phase 0 slope. They DECREASE THE AUTOMATICITY of the SA node and decrease AV nodal conduction velocity (increases the block at the AV node).
Calcium channel blockers
Class 4 AADs. Mostly affect the SA and AV nodal tissue. Overall effect is to decrease automaticity of the SA node and decrease AV nodal conduction. Names: Verapamil and Diltiazem.
NY Heart association classes of heart failure
Class I: ordinary physical activity does not cause undue fatigue or dyspnea. Class II: ordinary physical activity results in fatigue or dyspnea. Class III: less than ordinary physical activity results in fatigue or dyspnea. Class IV: symptoms and fatigue and dyspnea are present at rest.
Possible infectious endocarditis
Clinical (1 major+1 minor, or 3 minor)
Reentry
Conduction velocity is going, and the head chases the tail. Between the head and the tail is the excitable gap. The speed that the head chases the tail is the conduction velocity. The time that the cells recover is the refractory period. Note: Antiarrhythmic medications slow conduction velocity and prolong the refractory period in order to terminate macro/micro reentry circuits.
Tension pneumothorax
Could cause obstructive shock. air is trapped in pleural space with 1 way valve, so air/pressure builds up. Mediastinum is shifted, which impedes venous return. Symptoms: chest pain, SOB, decreased breath sounds. Treatment: needle compression, chest tube.
Venousthromboembolism: diagnosis
Diagnosis can be difficult because the signs and symptoms are non-specific. If VTE is suspected, you must do further testing. Labs: see if D-DIMER (a fibrin degradation product) is elevated. Imaging: CT angiography with IV contrast, or V/Q scan with radiolabeled agent given IV and via inhalation
Diuretics
Diuretics are used often in the treatment of SYMPTOMATIC heart failure with fluid retention. They do NOT improve long-term outcomes, but they relieve symptoms of volume overload (edema, dyspnea, lung rales, jugular distension, hepatomegaly, pulmonary edema (on xray)). They can be used long-term for symptomatic relief but they do not improve outcomes.
Initial treatment of hemodynamically stable monomorphic wide complex tachycardia
Do vagal maneuvers and give Adenosine first, because if it is an AV nodal depenent tachycardia, then giving adenosine or doing vagal maneuver may terminate the arrhythmia or pause the ventricular rate enough to better determine the cause of the arrhythmia.
Heart failure: treatments
Drugs for chronic use: ACE inhibitors, ARBs, Aldosterone blockers, Beta blockers, Endopeptidase inhibitors, Hydralazine/Nitrates and Digoxin/Diuretics (for symptomatic relief). Drugs for acute use: Diuretics, Nitrates, Natriuretic peptides, phosphodiesterase inhibitors, beta agonists. Devices: Defibrillators, bi-ventricular pacemaker, ventricular assistance devices. Surgeries: Revascularization for coronary disease, Mitral valve replacement/repair, ventricular reconstruction (not common anymore), & heart transplant
QRS complex
Duration: 60-120 ms (0.06-0.12 s or <3 small boxes). QRS complex is considered low voltage if height on limb leads is <0.5 mV and on precordial leads is <1 mV. Low-voltage QRS is caused by an impedance to electrical flow (large chest, air, fluid, infiltrative diseases). QRS complex has large voltage due to ventricular hypertrophy (left or right) (which can be pathologic or physiologic).
Changes in blood pressure during exercise
During exercise: increased systolic blood pressure, increased mean arterial blood pressure, and increased pulse pressure. There is no change in diastolic blood pressure.
Defibrillation
EKG shows no clear R or T waves. Shock is delivered anytime in the cardiac cycle.
Complications of endocarditis
EMBOLI (stroke, lung abscess, renal abscess, osteomyelitis), immunologic effects such as GLOMERULONEPHRITIS, local/cardiac effects (HEART FAILURE, CONDUCTION ABNORMALITIES, PERIVALVULAR ABSCESS). This might need very acute surgical interventions.
Venousthromboembolism: risk of recurrence
Elevated risk of recurrence in people with multiple VTE episodes, unprovoked VTE, women who continue OCP/hormone replacement therapy after a VTE episode, proximal vein thrombosis (in pelvis), elevated D-dimer level during or after anticoagulation discontinuation
Treatment of infectious endocarditis
Empirical treatment: treat based on what is most likely (S. aureus [MSSA/MRSA], Streptococci, Enterococci). Gram (+) is most likely. Is the valve native or prosthetic? Prosthetics are harder to great. For NATIVE VALVE: Vancomycin + Ceftriaxone (or other beta lactam). for PROSTHETIC VALVE: Vancomycin + Gentamicin + Rifampin. Treat with HIGH DOSE for a LONG TIME (4-6 weeks) to maximize pharmacodynamics. Use bactericidal drugs that can PENETRATE BIOFILMS (beta lactam antibiotics, which are safe at high doses unless patient has an allergy). We also give Vancomycin due to risk of resistance, but beta lactams are actually the better drug. Based on the culture results, look up the guidelines for treatment for the specific organism.
Pathophysiology of infectious endocarditis
Endocardial injury→platelet/fibrin reaction→transient bacteremia→microbial factors (biofilms, slimes)→vegetation→clinically evident endocarditis
Pericarditis: predictors of poor prognosis
Fever >38ºC, SUBACUTE onset, large PERICARDIAL EFFUSION, presence of CARDIAC TAMPONADE, lack of response to therapy, MYOPERICARDITIS (pericarditis+myocarditis), IMMUNOSUPPRESSION (for any reason), caused by TRAUMA, or on ORAL ANTICOAGULANT THERAPY.
Treatment for aortic stenosis
For aortic stenosis: there isn't good medical therapy, surgery is best option.
Treatment for mitral stenosis
For mitral stenosis, treat with diuretics, HR controlling agents (to prevent atrial arrhythmias and allow for increased ventricular filling time), Percutaneous Balloon Mitral Valvuloplasty (PBMV, in which a catheter is brought into the mitral valve and a balloon is opened to open up the stenotic mitral valve).
Long term maintenance of sinus rhythm
For patients without structural heart disease, give Class 1C agents (FLECAINIDE & PROPAFENONE). Can also give Class 3 agents (AMIODARONE, DRONEDERONE (safer alternative to Amiodarone, given if patient does not have heart failure), and DOFETILIDE& SOTOLOL (both have high risk of Torsades de Pointes, so these require 3 day hospital stay with careful EKG monitoring, renal monitoring, QT interval monitoring, and drug interaction monitoring)
Nutrient-drug interactions: Furosemide
Furosemide is potassium and thiamine depleting with long-term use, so increase dietary potassium
Empiric antibiotics for septic shock
Give antibiotics to cover both gram positive and gram negative bacteria (Zosyn and ceftriaxone or Imipenem). Add additional coverage as indicated (Gentamycin or Cefepime for pseudomonas, Vancomycin for MRSA, Clindamycin or Metronidazole for anaerobic infections, Ceftriaxone for asplenic individuals, Cefepime or Imipenem for neutropenic individuals) - don't think we need to know these details.
Starling curves
Graphs ventricular performance (aka cardiac output) vs End diastolic volume. In normal heart: stretching the heart more (by increasing EDV) results in increased cardiac output. This occurs during exercise (increased venous return to LV causes stretching of LV and cardiac output increases). When there is fatal myocardial depression, the myocardium does not increase its contractile ability upon stretch, and they always have high end diastolic volumes and low cardiac output. It can happen due to MI, viral infection, diabetes, alcoholism, and other causes. As a result of high end diastolic volume, there is high end diastolic pressure and high atrial pressure. This high atrial pressure backs up and causes pulmonary venous pressure and pulmonary edema. As a result, fluid leaks into the lungs. When EDV is very high, it causes this pulmonary edema.
Mitral stenosis
Gross image: there is DIFFUSE FIBROUS THICKENING and distortion of valve leaflets, FIBROUS BRIDGING OF VALVULAR COMMISSURES (bc it is almost always caused by rheumatic fever). There can be FISH MOUTH or BUTTONHOLE stenoses. LEFT ATRIUM progressively dilates. May harbor MURAL THROMBI in appendage or on the wall which can then embolyze. Long standing pulmonary congestion leads to pulmonary hypertensive changes and RV hypertrophy.
5 main causes of pulmonary hypertension
Group 1: pulmonary arterial hyptertension (treated with pulmonary arterial vasodilators). Group 2: Left heart related (systolic dysfunction, diastolic dysfunction, valvular disease such as mitral stenosis and mitral regurgitation). Group 3: lung/hypoxia related (COPD, interstitial lung disease, etc). Group 4: Chronic thromboembolic pulmonary hypertension (clots in lungs without DVT - this form is reversed by open heart surgery and pulmonary arterial embolectomy). Group 5: unclear/multifactorial mechanisms.
High fat DASH diet vs regular DASH diet
HF-DASH is higher in fat &lower in carbohydrates. there is similar reduction in BP between both diets, but HF-DASH diet significantly reduced triglycerides and VLDL. DASH diet significantly reduces LDL, HDL, apolipoprotein A-I (a protein component of HDL), intermediate density lipoprotein, and large LDL particles.
Heart failure clinical syndrome
Heart Failure is the pathophysiological state in which abnormalities of the entire cardiovascular system are responsible for the INABILITY TO DELIVER BLOOD (OXYGEN) at a rate COMMENSURATE WITH THE REQUIREMENTS of the metabolizing tissues leading to symptoms of DYSPNEA AT REST OR WITH EXERTION, and FATIGUE. Often accompanied with VOLUME OVERLOAD. This may occur in association with IMPAIRED SYSTOLIC FUNCTION (low ejection fraction) referred to as systolic dysfunction heart failure or IMPAIRED DIASTOLIC FUNCTION referred to as diastolic dysfunction heart failure (the latter often only clinically expressed in association with other co-morbidities). BOTH result in IMPAIRED CARDIAC OUTPUT.
Cardiac output AT REST (lying down)
Heart rate at rest is 60-100 BPM, and VAGAL tone predominates. Stroke volume is due to positional increase (due to lying down) of venous return. Stroke volume is maximal when lying down at rest (normal: 50-70 mL/beat) because venous return is maximal when lying down. Note: Well trained athlete has ENHANCED VAGAL TONE, so the resting stroke volume is increased (90-110 mL/beat), and resting heart rate is decreased (<50 BPM).
Changes that occur during maximum effort exercise
Heart rate increases due to sympathetic stimulation (pulmonary stretch receptors, circulating norepinephrine and epinephrine), and increased venous return (venoconstriction & skeletal muscle compression). HR is the more important adaptation during exercise, and HR increases until a maximum is reached. Stroke volume can increase to 110-130 mL/beat in normal people and then plateaus. Well trained athletes can have maximal stroke volume of 150-220 mL/beat
Changes in hemoglobin concentration during exercise
Hemoglobin concentration increases during exercise. It is due to DECREASED PLASMA VOLUME, so concentration of hemoglobin increases. It is NOT due to increased RBC production. As a result of increased hemoglobin concentration, there is INCREASED OXYGEN CARRYING CAPACITY and INCREASED OXYGEN DELIVER to working tissues.
Roth's spots
IMMUNOLOGIC complexes in the retina with local hemorrhage
High risk groups for developing endocarditis
IV drug users, artificial valves, cardiac devices, dental work/poor dentition, congenital heart disease with shunts, rheumatic heart disease, hypertrophic obstructive cardiomyopathy. Bacteria tend to attach to things that are not covered in endothelium: artificial valves, cardiac devices, other artificial hardware. Bacteria also tend to attach to places where the endocardium has been denuded by turbulent bloodflow (such as congenital shunts, hypertrophic obstructive cardiomyopathy)
Acute management of atrial fibrillation, atrial flutter, and atrial tachycardia
IV drugs to acutely manage HR: Beta blockers (Esmolol, Metoprolol, Propranolol), calcium channel blockers (Diltiazem, Verapamil), and Digoxin (oral or IV, especially in patients with systolic heart failure).
Acutely restoring normal rhythm
IV drugs: Ilbutilide (class 3 AAD, usually works within 90 minutes), Amiodarone (class 3 AAD, takes 24-48 hours). Oral drugs: Flecainide (class 1C) and Propafenone (1C) can be used for "pill in the pocket"
Determining if EKG has sinus rhythm
If P wave is upright in lead II and inverted in aVR, and each P wave is followed by a QRS, then it is sinus rhythm
Treatment for AV block
If level of block is His or below, advanced second degree, third degree, or if patient is symptomatic (at any level): treat with a pacemaker.
Treatment for Monomorphic ventricular tachycardia
If stable, treat with AMIODARONE (class 3) or LIDOCAINE IV (class IB). If patient has electrical storm, treat with sedation (to remove sympathetic innervation), IV beta blocker, IV amiodarone, AND IV lidocaine. Try to determine the underlying cause (electrical abnormalities, drug toxicity, coronary ischemia).
Early afterdepolarizations (EADs)
If there is a PROLONGED QTc, there can be EADs (another impulse can come when there is partial repolarization, which triggers an arrhythmia known as Torsades de Pointes). Can be due to a problem in phase 2 or phase 3 repolarization.
PV loop of diastolic dysfunction
In a heart with diastolic dysfunction, there is INCREASED CHAMBER STIFFNESS. For the same given volume, pressure will be higher (~23 mmHg). In normal patients, when end diastolic pressure (and LA pressure) is ≥25 mmHg, pulmonary venous pressure is also ≥25 mmHg. 25 mmHg is usually the threshold for developing pulmonary edema in normal patients. When end diastolic pressure is too high, the stroke volume must be decreased to compensate. As a result, there is decreased cardiac output.
Key differences between nodal and contractile tissue
In nodal tissue, the phase 0 depolarization is mediated by calcium. In contractile cells, phase 0 depolarization is mediated by sodium. In nodal cells, the phase 4 slope is steep. In contractile tissue, the phase 4 slope is flat.
Heart failure: treatment objectives
Increase survival & decrease morbidity. Relieve symptoms: improve quality of life (especially by improving exercise capacity). Reversing neurohormonal abnormalities. Prevent progression of HF. Reverse LV remodeling. We currently uses ACE inhibitors, ARBs, Aldosterone receptor blockers, beta blockers, and NO-enhancing drugs (in a subgroup of patients).
Sodium channel (pacemaker current) aka funny channel (I-f)
Is activated by repolarization and contributes to diastolic repolarization (phase 4) in pacemaker cells. It is enhanced by sympathetic stimulation and suppressed by vagal stimulation. Voltage-gated.
DASH diet vs high blood pressure medications
Low salt, heart healthy DASH diet is as effective as drugs for some adults with high blood pressure: ACE inhibitors, beta blockers, and CCBs on average reduce SBP by 10-15 mmHg. DASH diet reduces diet by 5-21 mmHg (depending on baseline blood pressure). Higher baseline SBP has better results from decreasing dietary sodium.
Mean arterial pressure
MAP = Cardiac output*SVR = HR*SV*SVR. Mean arterial pressure increases during exercise. Anything that increases cardiac output (stroke volume / heart rate) and systemic vascular resistance increases mean arterial pressure. During exercise, the increased heart rate plays most important role. Stroke volume also increases, but this does not play as big of a role.
Valves that get infected (most to least) in endocarditis
MITRAL>AORTIC>TRICUSPID>PULMONIC. Tricuspid endocarditis/right sided endocarditis is more associated with IV drug use. However, in general the left heart is more likely to be infected. Note: These numbers are changing: the mitral valve is currently most commonly infected, but lots of endocarditis in the past was driven by rheumatic fever. People don't really get rheumatic fever anymore, so incidence of mitral endocarditis is decreasing.
Subacute bacterial endocarditis
MORE INSIDUOUS and protracted/indolent course. LESS DESTRUCTIVE to the underlying valves. Less virulent organisms: STREP VIRIDANS or ENTEROCOCCUS. Typically infects deformed valves. With SUBACUTE bacterial endocarditis, there is less valve destruction than with ACUTE bacterial endocarditis. If not treated, usually fatal within 1 year. Symptoms: low grade fever, anorexia/weight loss, fatigue, nausea/vomiting, arthralgias/myalgias, abdominal pain
Treatment for valvular disease
Medical therapy (alleviates symptoms but does not prolong survival). Surgery options: Balloon valvuloplasty (PBMV: catheterization to insert balloon inside the mitral valve to open it up), surgical valve repair (done via sternotomy or thoracotomy, to allow the leaflets to work better and come together in a normal position), Valve replacement (bioprosthetic valves from pig, cow, or cadaver, Bileaflet valve).
Secondary pericardial masses
Mets from lung, breast, melanoma, and lymphoma can metastasize to the pericardium.
Mitral stenosis: clinical case symptoms
Mitral stenosis is usually caused by rheumatic heart disease. It is a longstanding disease that develops over years. Pregnancy is a relatively volume overload state (women double intravascular volume during pregnancy). When pregnant women exert themselves, not enough blood can get through the mitral valve, pressure in LA rises, pressure in pulmonary venous circulation rises, transcapillary pressure in lungs rises, which can cause transient PULMONARY EDEMA and DYSPNEA ON EXERTION. HOARSE VOICE (caused by dilation of LA). can also have difficulty swallowing and chest pain. HEMOPTYSIS (due to transudation of blood into lungs). PAROXYSMAL NOCTURNAL DYSPNEA (a marker of heart failure and it is caused by the accumulation of fluid in lungs when supine). LOUD S1 (because mitral valve does not open well, and when it opens it snaps) and loud P2 (because pulmonary vessels are at higher pressure), RUMBLING MID-DIASTOLIC MURMUR (due to flow accelerating through the narrowed valve), & opening snap. EKG can show RV hypertrophy. CXR shows enlarged left atrium
Aortic stenosis: clinical case symptoms
More common in elderly (calcific), EXERCISE INDUCED CHEST PAIN (because AS is accompanied with LVH. As the muscle becomes thickened, it requires a larger blood supply and higher O2 requirements. This results in angina on exertion). DYSPNEA ON EXERTION (LVH leads to increased LV pressure and LA pressure, which leads to INCREASED PULMONARY PRESSURES). SYNCOPE (cardiac output cannot increase during exertion because of the stenotic aortic valve). DELAYED, SLOW-RISING CAROTID UPSTROKE (pulsus parvus et tardus). SOFT/ABSENT S2 (a marker of severe aortic stenosis). Harsh late-peaking CRESCENDO-DECRESCENDO SYSTOLIC MURMUR loudest at 2nd right ICS that RADIATES TO THE CAROTIDS (because there is turbulent flow into the carotids). EKG most likely shows LVH (higher voltage of S wave and R wave). CXR shows calcifications at the aortic level, post-stenotic aortic dilation, and LVH.
Other presentations for infectious endocarditis
Multiple lung absccesses, multiple liver/spleen abscesses.
Pathophysiologic cascade in chronic heart failure
Neurohormonal abnormalities, adrenergic dysfunction, cytokine abnormalities, impairment in electrical function. Cardiac necrosis (due to MI or other cause) causes myocyte loss. There is a decrease in cardiac output which causes increased sympathetic tone (norepinephrine), which leads to vasoconstriction, increased blood pressure, and increased myocardial afterload. When the kidneys sense low blood flow (decreased cardiac output), they secrete renin, which ultimately activates angiotensin II. Angiotensin II is a potent vasoconstrictor, it mediates other neurohormones (Aldoesterone, ADH) which lead to increased sodium and water retention, AND it mediates the release of another potent vasoconstrictor, Endothelin. The salt/water retention and vasoconstriction together cause increased afterload on the already failing ventricle. There are increased levels of norepinephrine in circulation, and norepinephrine has direct cardiac toxic effects (beta receptor downregulation and energy starvation in the heart). Patients with heart failure have elevated levels of certain cytokines (including TNF). These cytokines activate oncogenes that mediate the process of apoptosis. In some patients, there is also marked decrease of NO production. NO is a vasodilator that would offset some of the vasoconstrictor neurohormones that are present. In 30% of patients there is electrical dysfunction, which worsens the underlying problem.
Sympathetic effect on HR
Norepinephrine is released from sympathetic neurons → activates beta1 receptors of autorhythmic cells → INCREASES SODIUM AND CALCIUM INFLUX → increases rate of depolarization → increases HR.
Vasoconstricting & sodium retaining neurohormones (bad)
Norepinephrine, Angiotensin II, Aldosterone, Vasopressin, Endothelin. Vasoconstricting, sodium/water retaining neurohormones overwhelm the system in patients with heart failure. As a result, the heart failure syndrome worsens progressively over time. The vasoconstricting & sodium/water retaining neurohormones are responsible for much of the morbidity and mortality of CHF.
Bicuspid aortic valve
Normal AV valve: 3 cusps. 1-2% of population has Bicuspid AV, so there is greater tendency to develop Aortic stenosis in these people. It is the most common cardiac congenital abnormality in humans, and the most common cause of AS in middle age.
Normal aortic valve
Normal aortic valve is 2-4 cm^2 (about size of US nickel). Stenotic aortic valve is <1.0 cm^2, and average pressure gradient throughout systole is >40 mmHg. The aortic valve is after the LV, which can create high pressure (~120 mmHg). If there is obstruction due to aortic stenosis, the pressure in the left ventricle has to be much higher to move the same volume of blood.
Normal mitral valve
Normal aortic valve is 4-6 cm^2 (about size of US quarter). Stenotic aortic valve is <1.5 cm^2, and mean pressure gradient is >10 mmHg (LA pressure is 10 mmHg higher than LV pressure during diastole)
Physiologic requirements of exercise
Normal cell structure/function, structurally normal heart, Effective increase in cardiac ouptut (HR and SV, but HR is more important), effective blood vessels that distribute blood flow to match local tissue gas exchange requirements (affected by SVR), proper functioning lungs, effective pulmonary circulation, ventilatory control mechanisms that can regulate arterial blood gas tensions and pH, neurohormonal functioning systems (sympathetic and parasympathetic), blood has normal hemoglobin concentration and adequate function. All of these are required for someone to exercise efficiently.
Valvular regurgitation
Normally there is unimpeded antegrade flow. There is a pathologic change that causes incomplete closure of valve leaflets, resulting in RETROGRADE FLOW during systole. There is VOLUME OVERLOAD of the upstream chamber as a result. Compensation occurs via increased compliance of the upstream chamber, and chamber dilation occurs.
Infective endocarditis
ORGANISMS COLONIZE OR INVADE HEART VALVES OR ENDOCARDIUM. Vegetations of THROMBOTIC DEBRIS AND ORGANISMS, often with destruction of the underlying cardiac tissues. BACTERIAL INFECTIONS are most common cause, but can be caused by fungi and other microorganisms. The aortic, aneurysm sacs, other blood vessels, and prosthetic devices can also become infected. Predisposing factors are CARDIAC AND VASCULAR ABNORMALITIES (mitral valve prolapse, calcific valvular stenosis, bicuspid AV, artificial valves, congenital defects, rheumatic heart disease*). Risk can be lowered with antibiotic prophylaxis. Pathogenesis: Organism can come from an infection anywhere, DENTAL OR SURGICAL PROCEDURE, contaminated needle (IV drug user), or trivial breaks in the epithelial barriers of the gut, oral cavity, or skin. Gross image: friable, bulky destructive vegetations on the heart valve. Can be single or multiple and involve 1 or more valves. Histology: VEGETATIONS (fibrin, inflammatory cells, bacterial colonies) and EMBOLI (containing bacteria and can cause abscesses to develop at sites where the emboli lodge). The emboli can cause SEPTIC INFARCTS or MYCOTIC ANEURYSMS (includes bacteria, not just fungi). Note: Any valvular vegetation on in the left heart (aortic and mitral valves) has the potential to embolize systemically. Left sided vegetations are much more serious than right sided vegetations for this reason.
Change in oxygen dissociation curve during exercise
Oxygen dissociation curve shifts to the right during exercise. Due to acidosis (lactic acid, CO2), increased temperature, increased CO2, and increased 2,3-BPG.
What comprises the PR interval
PA (firing of SA node until arrival at AV node), AH (arrival at AV node until meets the Bundle of His), His (conduction time through His), and HV (time between His bundle to ventricular contraction).
Risk factors/predisposing conditions for endocarditis
PAST ENDOCARDITIS (recurrence), Age >60 (50% of cases, due to senile changes to heart valves), male gender (more due to behavior), poor dentition, injection drug use, STRUCTURAL HEART DISEASE (valve disease, congenital heart disease, prosthetic devices), HEMODIALYSIS (portal of entry into central blood, especially with catheters, because there is large volume of exposure for bacterial infection), PICC line, pacemaker (basically anything synthetic). Predisposing condition: something that interrupts the endothelium to allow platelets/fibrinogen to aggregate, which bacteria can attach to and colonize there.
Major criteria for IE
POSITIVE BLOOD CULTURES from different veins (3 sets, and at least 2 are positive) which show "high grade" bacteremia, ECHOCARDIOGRAM (either transthoracic echo or transesophageal, which shows evidence of valvular damage). Note: L sided heart is more commonly effected, so the transesophageal (which goes behind the heart) is more sensitive.
First degree AV block
PR interval is >200 ms. Every P wave is followed by a QRS, but the interval between them is abnormally long. Caused by diseases of the AV node (usually benign, with minimal risk of progression to complete AV block).
Second degree type 1 AV block aka Mobitz 1 aka Wenchebach
PR interval is >200 ms. the p-p interval is regular, but not every P causes a QRS (grouped beating). The PR interval after the blocked beat should be shorter than before the blocked beat (the PR interval gets longer and longer and then there is a skipped beat). If these are true, you know it is 2nd degree AV block aka Mobitz 1. Caused by diseases of the AV node (usually benign, with minimal risk of progression to complete AV block)
Endocarditis prophylaxis
Patients who should be treated with prophylactic antibiotics before an invasive dental procedure: PREVIOUS ENDOCARDITIS, PROSTHETIC HEART VALVE, CARDIAC TRANSPLANT WITH VALVE DISEASE, or UNREPAIRED CONGENITAL HEART DISEASE. These guidelines are not followed well. Only the people at the MOST high risk should be prophylactically treated.
Common causes of pericardial effusion
Pericarditis, TUBERCULOSIS (common cause worldwide), iatrogenic (invasive-procedure related, post-cardiac surgery), trauma, neoplasm/malignancy
Nutrient-drug interactions: Spironolactone
Potassium sparing (may require restriction of potassium)
Behavior of accessory pathways
Pre-excitation (simultaneous conduction from A→V through both the AV node and the accessory pathway), AV nodal dependent (orthodromic or antidromic), or atrial fibrillation with uncontrolled conduction (BAD)
Factors that regulate cardiac output
Preload, afterload, heart rate, and contractility/inotropy
Mechanisms of arrhythmia
Problems with impulse generation: enhanced automaticity (an area of the cell goes rogue, and there is an exceptionally steep stage 4 slope, which generates an unpredictable rate of impulse without control by the body), or triggered activity. Problem with impulse conduction: reentry.
Bundle branch blocks
QRS is >120 msec (>3 small boxes). To diagnose left or right bundle branch block, look at V1 and V6.
Right bundle branch block (RBBB)
QRS is >120 msec (>3 small boxes). V1 has a very characteristic rSR' (there are 2 R waves) or rR' (the 2nd R wave does not dip below baseline before rising again). V6 shows broad, slurred S wave. This occurs because the conduction is moving fast down the left bundle branch and exits the Purkinje network, so the left ventricle contracts. The small r wave shows that the left ventricle has gotten its electrical impulse through the left bundle branch. However, the conduction was blocked in the right bundle branch (due to slowed conduction velocity, the right bundle branch is refractory to the next impulse, or there is collision of wavefronts from somewhere else). The LV contracts and the conduction spreads via gap junction from LV to RV (slower), and then the RV contracts.
Left bundle branch block (LBBB)
QRS is >120 msec (>3 small boxes). in V1, there is a deep, wide S wave (because the activity is in the left ventricle which is away from the V1 lead). In V6, there is a huge R wave (based on where the lead is placed on the chest). the majority of the delayed, slowed R wave is in V6, so it is a LBBB.
Acute bacterial endocarditis
RAPIDLY PROGRESSIVE & HIGHLY DESTRUCTIVE. Highly virulent and destructive organisms: STAPH AUREUS. Typically infects a previously normal heart. There can be metastatic foci. If not treated, usually fatal within 6 weeks. Symptoms: high grade fever/chills, SOB, arthralgias/myalgias (significant pains), abdominal pain, pleuritic chest pain, back pain.
Minor criteria for IE
RISK FACTORS, FEVER, blood cultures that do not meet major criteria, VASCULAR phenomena (major arterial emboli, septal pulmonary infarcts, mycotic aneurysm, intracranial hemorrhage, conjunctival hemorrhages, Janeway lesions, petechiae, Splinter hemorrhages), IMMUNOLOGIC phenomena (glomerulonephritis, Osler nodes, Roth spots, rheumatoid factor)
2 options for treating AV nodal dependent tachycardia
Rate control option (the atrium remains in the arrhythmia, but conduction down the AV node is slowed so the ventricles are not in arrhythmia. The ventricular rate is controlled to have resting HR <110 BPM), or Rhythm control option (the atrium is converted back to sinus rhythm. Medications are more powerful and they can maintain sinus rhythm. There is a higher risk of side effects (systemic toxicity, arrhythmogenesis))
Mitral regurgitation: clinical case symptoms
Recent MI (due to ischemia/rupture of papillary muscles), dyspnea, fatigue, new murmur, bibasilar crackles, PROMINENT S3 (caused by volume overload), PANSYSTOLIC MURMUR at the apex with radiation to axilla, Hyperdynamic LV impulse, no step-up in blood O2 from RA to pulmonary artery, and giant V waves on venous pulsations (because the RA is filling even more than usual). CXR of severe chronic MR shows hugely enlarged heart.
Replacing saturated fat with polyunsaturated fat (linoleic acid)
Replacing saturated fat with polyunsaturated fat (linoleic acid) is linked to lower risk of CVD. Research found that replacing 5% of calories consumed from SATURATED FAT with LINOLEIC ACID (found in vegetable oil, nuts, and seeds) lowered risk of coronary heart disease by 9% and overall risk of death from CHD by 13%.
Endocarditis: history and physical
Risk factors: cardiac lesions (problems with heart valve), devices (which can allow a nidus for infection), behavioral risk factors. Physical exam: MURMUR, (either due to damage by the infection or damage that predisposed patient to get endocarditis), EKG, Stigmata (Janeway's lesion, Osler's node, splinter hemorrhages)
Pre-excitation via accessory pathway
SA node sends impulse out→impulse gets sent via both the AV node and the accessory pathway. EKG shows P wave with short PR interval (<120 ms). There is also a delta wave (the R wave is angled and then steep, due to conduction through the accessory pathway). This can occur with or without Wolff Parkinson White (WPW) syndrome
Most common organism that causes infective endocarditis
STAPH AUREUS IS by far the #1 organism that causes infective endocarditis. It is increasing due to HEALTHCARE ASSOCIATED INFECTIONS, prosthetic device infections, and by venous access. S. aureus lives on the skin, so it easily infects the bloodstream if there are breaks in the bloodstream. It causes a very severe, fulminant/acute infection.
Other common organisms that cause IE (from most to least common)
STAPH AUREUS, Viridans streptococci, Enterococci. It can be lots of different organisms. 85% are GRAM POSITIVE.
Recurrent pericarditis: treatment
Same medicines are used, but for longer time. INDOMETHACIN is also added. It is the most potent oral anti-inflammatory medication that is used. It has many side effects (especially on kidneys) so it is not used for acute pericarditis. COLCHICINE is given for at least 6 months for recurrent pericarditis. Aspirin or Ibuprofen is given for weeks-months. Second line: low-dose corticosteroids (if non-bacterial/infectious). Third line: Immunomodulatory therapy (immunoglobulin or anakinra or azathioprine). Fourth line: Pericardiectomy.
Cardiac myocyte ion concentrations
Sodium: higher extracellularly (When sodium channels open, sodium flows from outside→inside, which generates inward current i.e. DEPOLARIZATION). Potassium: higher intracellularly (When potassium channels open, potassium flows from inside→outside, which generates outward current i.e. POLARIZATION). Calcium: higher extracellularly (When calcium channels open, calcium flows from outside→inside, which generates inward current i.e. DEPOLARIZATION). Chloride: hgher extracellularly (When chloride channels open, chloride flows from outside→inside, which generates outward current i.e. POLARIZATION)
AADs that are renally excreted
Sotalol, Digoxin, and Dofetelide. Sotalol and Dofetelide both require 3 day hospital stay and can only be given to patient with good renal function.
Guidelines for surgical intervention for infectious endocarditis
Surgery is indicated when there are large vegetations (unable to be controlled medically), high risk of embolization, severe valve dysfunction, abscess, persistent infection
Heart failure: symptoms
Symptoms: dyspnea on exertion, fatigue. Symptoms are due to pump dysfunction→neurohormonal activation and peripheral remodeling→end organ hypoperfusion→decreased O2 delivery. Additional symptoms (secondary to volume overload): Orthopnea (shortness of breath with lying flat), Paroxysmal nocturnal dyspnea (being awoken from sleep at night choking and unable to breathe), pulmonary edema, peripheral edema. PALPITATIONS (irregular rhythms and tachycardias), nocturia, confusion, disorientation from cerebral hypoperfusion, GI/RUQ discomfort (hepatic capsule distension), anorexia, nausea.
Decrimental properties
The AV node exhibits decrimental properties: the faster the atrium rate, the slower the AV node. It occurs to protect the ventricle from unopposed stimulation in the atrium (it protects the ventricle from too much atrial activity). However, accessory pathways do not exhibit decrimental properties, and they can conduct in either direction (A→V and V→A) and they can be very problematic.
Atrial pacing
The EKG machine has ways to filter out electrical pacing spikes. It shows pacemaker spikes as sharp vertical lines before the P wave (for atrial pacing).
Overdrive suppression
The fastest pacemaker drives the heartrate and suppresses the activity of the other pacemakers. When the SA node is serving as the primary pacemaker, the other pacemakers are suppressed. When an ectopic pacemaker is the fastest, it suppresses the other pacemakers.
Pacemaker potential in nodal cells
The pacemaker fibers do NOT exhibit a steady resting membrane potential, they exhibit a slow depolarizing phase 4. This is due to 2 components: The lowest membrane potential (-65 mV) is reached upon repolarization (due to INWARD RECTIFIER POTASSIUM CHANNEL current, IK1). The slow steady depolarization that brings the membrane potential towards the threshold is due to slow influx of sodium through FUNNY CHANNELS (aka FUNNY CURRENT). The latter portion of this phase is also due to the influx of calcium through L-TYPE and T-TYPE CALCIUM CHANNELS
Anticipation of dynamic exercise
There is a Slight SYMPATHETIC SURGE (release of epinephrine and norepinephrine from adrenals, HR increases, vagal tone decreases, increased venous return [PRELOAD] due to sympathetic-mediated venoconstriction). The goal is to increase resting cardiac output BEFORE exercise even starts.
Changes during Dynamic exercise withdrawal
There is withdrawal of sympathetic tone and return of parasympathetic tone. HR decreases, SVR takes a while to increase (due to persistent vasodilation in skeletal muscle), and systolic BP falls below baseline for up to 12 hours. Mechanoreceptors take over in stabilizing adequate perfusion pressure until the peripheral effects wear off.
Torsades de Pointes vs polymorphic ventricular tachycardia
Torsades de Pointes is initiated by 1) long QT interval, 2) pause in the cycle, 3) premature beat during a T wave, resulting in polymorphic ventricular tachycardia. Caused by early afterdepolarizations.
Evaluating a patient in shock
VITAL SIGNS (including rectal temp), CARDIOVESPIRATORY MONITOR, Pulse ox, SUPPLEMENTAL OXYGEN, IV access. Take an accurate history! (from bystanders or family). Physical exam, lab tests, ARTERIAL BLOOD GAS.
Factors that affect cardiac preload
Vascular resistance (especially VENOUS vascular resistance. If venous vascular resistance ↑, then cardiac preload ↑). Venous capacitance (volume of blood stored in venous circulation, so ↓ venous capacitance ↑ cardiac preload), and ventricular filling time (if HR is >150-200, then the heart spends less time in diastole so cardiac preload is ↓).
Sympathetic effects during exercise
Venoconstriction (increases cardiac preload) & arterial vasoconstriction (increases afterload). HR increases. Sympathetic output causes sweating.
Factors that affect venous return
Venous return is determined by the difference between the peripheral and central venous compartments. Decreased peripheral venous pressure may result from: blood loss by hemorrhage, loss of body fluid through severe sweating, diarrhea, or vomiting, and venodilation. Increased peripheral venous pressure may result from: blood transfusion, fluid retention in the kidneys, increase in circulating blood volume, venoconstriction, venous compression, exercise, and wearing elastic stockings.
Effect of hemorrhage on cardiac and vascular function curves
When a patient hemorrhages: 1) there is a decrease in blood volume, so a new venous return curve is drawn. 2) there is increased sympathetic activity, which increases inotropy and chronotropy rapidly, so a new cardiac output is drawn. 3) there is venous constriction (also due to sympathetic activity), so venous capacitance decreases and venous return increases. Overall effect after these responses have occured: central venous pressure is slightly decreased but it is still within the normal range. Cardiac output/venous return are close to normal. The body was able to restore normal cardiac output because of sympathetic stimulation on the heart and venous vessels.
Complications of endocarditis
When bacteria infect the valves, immune cells also invade the area and cause damage attached to the valve. If the infection is degrading the valve, it can cause the valve to become incompetent (leaky), and if the infection is very aggressive it can perforate the valve (punch a hole) in the valve. Local complications: MURMUR (due to valvular regurgitation, perforation, flail/prolapsed leaflet, abscess), CONDUCTION ABNORMALITIES (AV block, generally permanent. due to the proximity of the valves to the conduction system), and HEART FAILURE (valvular abnormalities cause pump to become weak). Distant complications: EMBOLIC EVENTS (brain, spleen, kidneys, heart, extremities, lungs), Janeway lesions, Osler's nodules, splinter hemorrhages, Roth's spots on retina, splinter hemorrhages on nails, Splenomegaly)
Cardiomyopathy
a PRIMARY abnormality of myocardium. Wide array of etiologies: inflammation, immune, genetic, metabolic, idiopathic. Can be DILATED, HYPERTROPHIC, or RESTRICTIVE (stiff) based on morphology and function. Traditionally excludes ischemic causes.
Swan-Ganz catheter
a catheter that is placed in the heart to monitor hemodynamic status. It is used to determine pulmonary capillary wedge pressure aka Left atrial pressure, which is the CARDIAC PRELOAD
Spironolactone aka Aldactone
a competitive antagonist of the aldosterone receptor, and it blocks the effects of aldosterone. Spironolactone (on top of ACE inhibitors) has improved long-term survival compared to ACE inhibitor alone.
Aldosterone
a corticosteroid that is released by the adrenals through direct stimulation by Angiotensin II. It causes SALT AND WATER RETENTION, leading to edema. It also causes electrolyte abnormalities (low K and Mg, which can contribute to developing ARRHYTHMIAS). It also mediates FIBROSIS in the myocardium and blood vessels.
Cardiac cycle
a cycle of contraction and relaxation (with respect to changes in the ventricle). Atrial systole (atrial contraction), Ventricular systole (isovolumetric contraction→early rapid ventricular ejection→later slow ventricular ejection), and Ventricular diastole (isovolumetric relaxation→early rapid ventricular filling→later slow ventricular filling)
Defibrillator
a device used to prevent/treat ventricular arrhythmias. Half of patients who die of systolic heart failure die due to ventricular arrhythmias. Devices that can abort ventricular tachycardia or ventricular fibrillation by shocking the heart have been shown to improve long-term outcomes. Both of these studies show that defibrillators compared to conventional (medical) therapy improves the survival of patients with low ejection fraction heart failure. Indications: if patient's ejection fraction is <35%, they get a defibrillator. If patient has EF <35% and LBBB→they get combined defibrillator and biventricular pacemaker.
Compression ultrasound
a fast and easy test in which the veins of the groin and popliteal area are compressed. Normally, veins are larger than arteries. If the ultrasound is able to completely compress the vein, then the thrombus is not there. If the vein is not able to be compressed, then it is due to a thrombus within the vein. It is a useful tool to diagnose DVT.
Ventricular assist device
a flow device that takes flow from the left ventricle and pumps it through the machine and into the aorta. It is placed in the abdominal wall or peritoneal cavity. New generation ventricular assist devices are much smaller. Pulsatile flow device uses a motor (Blood is pulled in through one-way valves and pumped out through one-way valve into the aorta. These are not really used anymore bc continuous type is now preferred). Continuous screw-type LVAD (Blood is pulled in by rapid rotation of the screw, and blood is pumped through continuously into the aorta. You cannot measure systolic & diastolic BP because there is continuous flow of blood). Newer devices are called partial ventricular assist devices aka micro pump (very small device that pulls blood out of the left atrium and pumps it into the brachiocephalic artery (about 3 L/min). They are easier to put in than the bigger devices and they provide support to augment what the heart is doing)
Acute clinical syndrome of heart failure
a hemodynamic problem, the severity of which is a consequence of the degree of LV dysfunction and the rate at which it occurs, but NOT due to the underlying pathophysiologic alterations. Example: heart failure associated with MI.
Insufficient/regurgitant/incompetent valve
a leaky valve closure. The murmur will be heard when the valve should be closed.
Short PR interval (<120 ms)
a marker of conduction to the ventricle through a bypass tract
T wave
a marker of ventricular repolarization. Normal: the T wave is in the same direction as the QRS. There are different T wave morphologies: Nonspecific changes (biphasic, notched, broad/slow, flat) and other abnormalities (hyperkalemia, ischemia, strain, prolonged QT interval).
Stenotic valve
a narrowed valve opening. A murmur will be heard when the valve should be fully open.
Sodium channel (fast) (I-Na)
accounts for phase 0 of the action potential in CONTRACTILE cells. Its inactivation may contribute to phase 1 of the action potential. Voltage-gated.
Delayed afterdepolarization (DAD)
after the cell has fully repolarized, there is another stimulus that causes a delayed afterdepolarization. It is usually due to CYTOSOLIC CALCIUM ACCUMULATION. Can be caused by DIGOXIN TOXICITY.
Negative inotropic agents
agents that ultimately decrease the availability of calcium and therefore decrease contractility. Includes toxins, anesthetics, beta-adrenergic receptor blockers, calcium channel blockers
Positive inotropic agents
agents that ultimately increase the availability of calcium and therefore increase contractility. Includes cardiac glycosides (Digoxin, a Na/K ATPase blocker), adrenergic agonists, calcium channel agonists, phosphodiesterase inhibitors
DASH diet
aim to increase vegetables, fruits, whole grain intake, low fat dairy products, beans, poultry, vegetable oils. Avoid saturated fats, processed foods, and foods that are high in sodium (deli meats, high preservatives, longer shelf lives). Note: RDA for sodium is 2300 mg/day
Long PR interval (>200 ms)
aka AV block (a block in conduction between the atria and ventricles). Could be a block in the AV node, His, or below the His. Diseases of the AV node are the most common location of AV block.
Isotonic exercise
aka dynamic exercise. muscle contraction of large muscle groups that results in MOVEMENT and primarily places a VOLUME load on the heart. It causes venoconstriction and increases venous return (preload) to the heart. It increases cardiac output, increases oxygen consumption, REDUCES systemic vascular resistance
Isometric exercise
aka static exercise. constant muscular contraction of smaller muscle groups WITHOUT MOVEMENT and results in more PRESSURE than volume load on the heart. Example: during yoga when you are maintaining a position. The muscle is maintained in a tense state, which increases the pressure and increases afterload, which increases the pressure load of the heart. There is minimal change in cardiac output and oxygen consumption, and INCREASES systemic vascular resistance.
Automaticity
all myocardial cells have the ability to generate their own impulse. Normally, the SA node drives the pace of the heart. When an abnormal foci takes over, this abnormal focus dictates and dominates the pace of the heart. Enhanced automaticity is mediated by phase 4 slope.
Rheumatic fever
an ACUTE, IMMUNOLOGICALLY MEDIATED multisystem inflammatory disease that occurs a few weeks after group A streptococcal pharyngitis.
Relative refractory period (RRP)
an action potential can be fired with a larger-than-normal stimulus, but the shape of the action potential will be abnormal.
Ventricular arrhythmias
an arrhythmia that originates in the ventricles. Includes: ventricular tachycardia (can be monomorphic or polymorphic) and ventricular fibrillation.
Supraventricular arrhythmias
any arrhythmia that originates above the level of the ventricle. From most common to least common: Atrial fibrillation, atrial flutter, AV nodal reentry tachycardia, accessory pathway, atrial tachycardia
Consequence
any valvular disease that imposes LOAD onto the UPSTREAM cardiac chamber(s). If there is pathological change that leads to narrowing of the valvular orifice, there is IMPEDED ANTEGRADE FLOW which causes COMPENSATION to occur (increased pressure in the upstream chamber). The pressure of the upstream chamber increases, leading to PRESSURE OVERLOAD.
Pulsus paradoxus
arterial blood pressures decrease by ≥10 mmHg during inspiration (which can be determined by arterial line tracing or blood pressure cuff)
Nutrient-drug interactions: Statins
avoid grapefruit/grapefruit juice (it intereferes with the body's ability to metabolize statins, so statin levels can reach toxic levels)
Frank-Starling relationship
based on the length-tension relationship of single cardiac myocyte and sarcomere length. The volume of blood ejected by the ventricle depends on the volume of blood present in the ventricle at the end of diastole. When venous return increases, end diastolic volume increases and stroke volume increases. This relationship between EDV and stroke volume remains linear until very high levels of EDV are reached. The force that the muscle is able to develop for contraction is related to the ventricle filling and the stretch on the myocyte.
Type 2 AADs
beta blockers
Changes in blood plasma volume during exercise
blood plasma volume decreases by 10-20% by prolonged exercise. This is due to increased systolic blood pressure, changes in intramuscular osmotic pressures, and water from the intravascular compartment moves to the interstitial space.
Atrial tachycardia
can be caused by any of the 3 types of arrhythmogenesis (enhanced automaticity, triggered activity, or reentry). Anywhere in the atrium can be the driving force of atrial tachycardia. Atrial tachycardia can be regular or irregular, and it can have clear P waves or hidden in QRS or T waves. EKG: It is NOT sinus tachycardia. It is an ectopic atrial focus or atrial tachycardia (NOT triggered by SA node)
Left sided heart failure
can be caused by ischemia due to MI, hypertension, aortic stenosis, mitral regurgitation. The heart can't keep up with venous return from the lungs, so there is increased back pressure into the lungs that leads to PULMONARY CONGESTION AND EDEMA. Lungs sound heavy/wet (RALES). Microscopy of lungs shows congestion, edema, and Hemosiderin-laden macrophages ("heart failure cells") in the alveoli. When renal perfusion is decreased, there is increased activity of the Renin-Angiotensin-Aldosterone system, leading to retention of salt and water, which worsens the pulmonary edema. Can also result in hypoxic encephalopathy.
T wave inversion
can be due to ischemia
ST segment depression
can occur due to myocardial ischemia, reciprocal changes, and in when in V1 & V2 they can be POSTERIOR ST ELEVATION (in the setting of an inferior wall STEMI)
Acute rheumatic carditis
can occur with rheumatic fever. It is common during the active phase of RF and may progress to CHRONIC RHEUMATIC HEART DISEASE (RHD) and deforming fibrotic valvular disease. It is essentially the only cause of MITRAL STENOSIS. Histology: INFLAMMATION and ASCHOFF BODIES (at any layer of the heart: pancarditis=pericarditis, myocarditis, or endocarditis). Aschoff bodies are granuloma-like lesions made up of "caterpillar cells." Gross image: VERRUCAE (small vegetations/holes overlie necrotic foci along lines of closure). There is fibrinoid necrosis within the cusps or along chordae.
Carcinoid heart disease
carcinoid tumor is a tumor of neuroendocrine cells that can lead to a type of heart disease. It is seen in 50% OF PATIENTS with Carcinoid syndrome (most commonly in GI tract, lung, but can be anywhere). Leads to disease on the RIGHT SIDE of the heart: TRICUSPID INSUFFICIENCY (with or without pulmonary valve insufficiency), RIGHT SIDED STENOSIS. These tumors secrete a lot of BIOACTIVE PRODUCTS, and when these products accumulate in the blood, patients can get carcinoid syndrome. These products are broken down in the liver and lung. It tends to spare the left heart because these products are broken down in the lung, but they can involve the left sided valves if there is right→left shunting, lung tumor, or serotonergic drugs. Gross findings: the bioactive products stimulate smooth muscle cells to proliferate, and there is lots of fibrosis in response. There is significant scarring of the valves, endocardial surface, and occasionally in the IVC and pulmonary artery.
Cardiac excitation-contraction coupling
cardiac action potential→calcium enters the cell through voltage-gated calcium channel (L type calcium channel) during plateau phase→there is calcium-induced calcium release from the SR (via Ryanodine receptor) → calcium binds to troponin C on myofilaments→cross bridge cycling→muscle tension. Calcium reuptake occurs via the SR calcium ATPase pump (to the SR) and the sodium-calcium exchanger (to the extracellular space)
Effects of fiber intake on lipids
cardiovascular risk assessment is based off non-HDL cholesterol and ApoB (major protein of VLDL & LDL). Beta-glucan fiber (found in oatmeal and oat bran) has been shown to reduce LDL, Non-HDL, and ApoB.
Vagal maneuvers
carotid sinus massage, valsalva. bearing down causes increased parasympathetic tone to slow AV nodal conduction. These are maneuvers to lower HR if a patient has AV NODAL DEPENDENT TACHYCARDIA, but should only be done if the patient is hemodynamically stable.
Transudate
caused by increased systemic venous pressure
Chronic mitral regurgitation
caused by mitral valve prolapse (myxomatous degeneration of leaflets so that the leaflets get stretchy), severe LV dilation, papillary muscle dysfunction (due to ischemia), rheumatic heart disease, or endocarditis
ST segment elevation
caused by myocardial infarction and pericarditis.
Sarcoid myocarditis
caused by non-caseating granulomas of unknown etiology. Diagnosed by MRI and nuclear scan. Endomyocardial biopsy may be negative due to spotty myocardial distribution (so it is done less often). Treatment: CORTICOSTEROIDS alone or with Azathioprine or Cyclosporine
Acquired aortic valve bicuspid deformity (RVD)
caused by rheumatic fever. There is a FUSED COMMISSURE.
Acute mitral regurgitation
caused by rupture of chordae tendineae or papillary muscle, endocarditis, or trauma (blunt chest injury, stab wound).
Delayed rectifier potassium channel (I-K)
causes phase 3 of the action potential in both pacemaker and contractile cells. Is enhanced by increased intracellular calcium channel. Voltage gated.
Potassium channel blockers
class 3 AADs. All cause prolongation of the refractory period which can lead to prolonged QT intervals and Torsades de Pointes. The only exception is AMIODARONE. Overall effect of blocking the potassium channel is to PROLONG REPOLARIZATION.
Venousthromboembolism: symptoms
clinical signs and symptoms are non-specific. DYSPNEA, PLEURITIC CHEST PAIN (worse with breathing), pre-syncope, syncope, and/or hemoptysis, unilateral leg pain, signs of DVT (unilateral leg pain/swelling/redness). Pleuritic chest pain occurs because if the blood clot moves distally it can infarct the lung, which leads to cellular infiltration by inflammatory cells, and inflammation on the visceral layer of the pleura rubs on the parietal layer of the pleura during inhalation, leading to pain. However, many people wit a VTE have normal spO2, normal arterial oxygen gradients, and normal EKG.
Cardiac tamponade
clinical signs include breathlessness, fatigue/malaise, tachycardia, HYPOTENSION, RAISED JVP, MUFFLED HEART SOUNDS, PULSUS PARADOXUS. On EKG: ELECTRICAL ALTERNANS (because the heart is swinging within the pericardial space). On CXR: enlarged cardiac silhouette. The triad of hypotension, raised JVP, and muffled heart sounds should make you think of cardiac tamponade.
Anaphylactoid reaction
clinically indistinguishable from anaphylaxis, but does not require a sensitizing exposure and is not IgE mediated.
Resistance exercise
combination of isometric and isotonic exercise that produces contraction with movement
Calcific stenosis of congenitally bicuspid aortic valve
congenital bicuspid aortic valve is the most common cardiovascular malformation (1%). Late complications of this malformation are aortic stenosis or aortic regurgitation, infective endocarditis, aortic dilation and/or dissection, and cusp prolapse. There are also commonly structural abnormalities of the aortic wall. The mitral valve is generally normal. The bicuspid aortic valve tends to undergo calcific stenosis much earlier because the RAPHE (fusion location of cusps) is a major site of calcium deposits.
Pericardium
consists of 3 layers: the VISCERAL layer (which borders the myocardium), the PARIETAL layer, and FIBROUS layer. Between the parietal and visceral layers is a POTENTIAL SPACE which has fluid that lubricates the heart. The pericardium fixes the heart to the mediastinum, and it also acts as a barrier to prevent infection from getting to the heart.
Effective refractory period (ERP)
consists of the absolute and relative refractory periods. A normal action potential cannot occur during this phase
Chronic phase of myocardial damage during myocarditis
continued myocyte destruction via AUTOIMMUNE mechanisms and abnormal expression of human leukocyte antigen (HLA) in myocytes
Cardiac mechanics
contractile events of the heart. Includes length-tension relationship and force velocity curves related to the ability of the muscle to shorten and the afterload that the muscle is exposed to
Transient outward potassium channel (I-to)
contributes to phase 1 of the action potential. Voltage gated
L-type calcium channel (I-Ca-L)
contributes to phase 2 of the fast response action potential in contractile cells. Its inactivation may may contribute to phase 3 of the action potential. It causes phase 0 in PACEMAKER cells. Voltage-gated.
Cardiac tamponade
could cause obstructive shock. blood in the pericardial sac prevents venous return and function of the heart. Can be related to trauma, pericarditis, or MI. BECK'S TRIAD of symptoms: Hypotension, muffled heart sounds, JVD. Diagnosis: large heart on CXR, echo. Treatment: Pericardiocentisis.
Pulmonary embolism
could cause obstructive shock. if someone has underlying hypercoagulable state (cancer, hormone replacement therapy, immunocompromise, genetic causes) and there is venous stasis (long flight, etc). Virchow triad of causes: hypercoagulable, venous injury, venostasis. Signs: tachypnea, tachycardia, hypoxia. Tests: D-dimer, CT chest scan or VQ chest. Treatment: Heparin, consider thrombolytics
Rheumatic aortic stenosis
cusps are thickened and distorted, COMMISSURES ARE FUSED. Accounts for less than 10% of cases of AS.
Splinter hemorrhages
dark spots under fingernails which are due to microscopic emboli, and there is some transudation of bloodflow out of the capillary blood, causing hemorrhages
Hypertrophic cardiomyopathy
determined by genetics. There is left and/or right ventricular hypertrophy, sometimes asymmetric and usually involves the interventricular septum. Mutations in cardiac muscle proteins cause the disease in many patients. It is associated with diastolic heart failure (bc the ventricle is so small due to the hypertrophic ventricle walls).
Chronic syndrome of heart failure
determined not only by LV function but also by the relative severities and interplay of the underlying pathophysiologic alterations. Heart failure clinical syndrome starts with pump dysfunction, but it mediates downstream effects that are responsible for much of the morbidity and mortality that is seen in patients with heart failure. Note: When we talk about congestive heart failure, we are referring to the chronic illness, not the acute illness.
Mediterranean diet
diet characterized by high fiber, unsaturated fatty acids, and antioxidants. It is PLANT-BASED (fruits and vegetables, whole grains, legumes, nuts). Butter is replaced with healthy fats such as olive oil and canola oil (MUFA aka omega 3s). Uses herbs and spices instead of salt to flavor food. Red meat is limited, and fish/poultry is at least twice per week. Red wine in moderation (optional).
diet recommendations for people with hyperlipidemia
diet that is restricted in SATURATED FATS (<6% of calories should come from saturated fat, which is often found in animal meat and fried food) and 200 mg cholesterol/day diet (controversial). They should also have HIGH FIBER DIETS (35 g/day for men, 25 g/day for women)
Dilated cardiomyopathy
dilation and impaired contraction of the left or both ventricles, which is often associated with systolic dysfunction. Caused by viral, immune, alcohol, other toxic, familial, genetic, or unknown factors, or it is associated with recognized cardiovascular disease such as CAD, MI with loss of muscle function.
Acute phase of myocardial damage during myocarditis
direct cytotoxicity & cell mediated cytotoxicity leads to the release of toxic cytokines, which causes myocardial damage/dysfunction
Bradycardic arrhythmias
diseases of the SA node, AV block (1st degree, 2nd degree types 1 and 2, 3rd degree, and bundle branch blocks)
Pericardial window
done by CT surgery, in which a small subxyphoid incision is made in the anterior chest and then the pericardium is incised. The pericardium is drained to the left chest, so that fluid cannot accumulate in the pericardium. Fluid collects in the pleural space instead, which has a greater surface area to allow the fluid to reabsorb better. It prevents cardiac tamponade from recurring.
peaked T wave
due to hyperkalemia (high K)
Cardiac drift
during prolonged exercise, due to an increase in core body temperature, there is a gradual increase in the steady state HR
Polymorphic ventricular tachycardia
each beat looks different. There is PROLONGED QT INTERVAL. Can be due to medications or congenital.
Treatment of myocarditis
early identification (EARLY BIOPSY to rule out giant cell, eosinophilic, and sarcoid causes, which have specific treatments). RESTRICTION OF PHYSICAL EXERTION until inflammation has abated (i.e. when MRI/EMB/cardiac function have normalized, because exercise may promote arrhythmias). Treatment is SUPPORTIVE (ACE inhibitors, Angiotensin receptor blockers, Angiotensin Receptor-Neprilysin Inhibitors, Beta blockers, Aldosterone inhibitors, diuretics). Give a Life Vest (wearable defibrillators) or longer-term ICD/CRT device. Give balloon pumps/Impellas/transplant if symptoms are more severe. May be a role for stem cell transplants in the future. Treatment beyond the standard therapies for heart failure are controversial for lymphocytic form.
Heart failure: labs & diagnostics.
elevated liver enzymes (AST, ALT, LDH, due to congestion), abnormal renal function (increased BUN/Cr due to hypoperfusion), and hyponatremia (low sodium due to free water retention). CXR: cardiomegaly, perivascular edema, alveolar edema, congestion, and hazy pattern throughout lung fields due to interstitial edema. EKG may show patterns of prior MI and/or hypertrophy. Echo: shows heart size and function, wall motion abnormalities, and valvular pathology/function. Cardiac catheterization: invasive procedure done to see the coronary arteries. It can also be used to directly measure cardiac output and filling pressures.
Osler's nodules
erythematous and PAINFUL small nodules on the hands. They are painful because they are caused by the body's IMMUNOLOGIC response to the embolism. Generally develop due to SUBACUTE endocarditis. They are usually culture negative (because they are caused by immunologic response that causes LOCAL VASCULITIS)
Janeway lesions
erythematous, blanching, painless/nontender macules on palms and soles. Caused by local septic microemboli. Tend to be from ACUTE endocarditis and they usually culture positive.
Endocarditis due to IV drug use
estimated to cause 2-4 cases/1000 patient/years. Occurs more commonly in younger people, more in males than females (because males use more IV drugs). Higher percentage of RIGHT SIDED LESIONS, but left sided lesions can also occur. COIFECTIONS - lots of other infections can be transmitted by a dirty needle (HIV, hepatitis B & C). Many of the "stuff" in injection street drugs is not soluble. When it is forced through the heart at high pressure, it causes damage to the heart valves (like a sandblaster). After sandblasting the heart valves, the skin flora (from the injecting) can now colonize the damaged valve. Most common organisms: Staph aureus (skin/soft tissue infections), any gram (-), Viridans group Streptococci (poor dentition), Candida (it is found on all citrus fruits, and drug users use citrus fruits because the drugs dissolve better in acid)
Vegetarian diet
excludes meat products (red meat, poultry, fish) and byproducts of animal slaughter. There are several variations of vegetarian diet (ovo-lacto vegetarian, ovo vegetarian, lacto vegetarian, vegan)
Why does the heart fail?
failure of the pump, obstruction to flow, regurgitant flow (leakage backwards makes the heart work harder and eventually fail), disorders of conduction, & Disruption of the continuity of the circulatory system (such as aortic aneurysm rupture).
Left atrial pressure curve
has 3 main peaks: A wave, V wave, and C wave. A wave: results from ATRIAL CONTRACTION, which causes a small increase in pressure in the LA. At the end of the A wave, the mitral valve closes. C wave: after the mitral valve clsoes, there is another small peak in LV pressure due to cardiohemic vibrations caused by closing of the mitral valve. V wave: occurs when gradual filling of the LA has reached its peak, just before the mitral valve opens.
Pulmonary hypertension
has many different causes. Typically leads to increased blood pressure in the lungs and therefore increased workload for the right side of the heart. Eventually the right heart becomes enlarged and less able to pump blood through the lungs, which leads to progressive heart failure and ultimately death. Normal pulmonary vessel pressure is 8-20 mmHg. pulmonary HTN has pressure >25 mmHg at rest.
ACE inhibitors
have become a cornerstone of therapy for treatment of patients with low ejection fraction HF (systolic HF). They have 2 effects: 1) They block the conversion of angiotensin I → angiotensin II. 2) Prevent the breakdown of bradykinins. Bradykinins are prostaglandins which are broken down by the enzyme KININASE 2, and ACE inhibitors prevent the formation of kininase 2 which prevents the breakdown of bradykinin (Bradykinin is a vasodilator). Side effects: cough, angioedema (swelling of face and tongue, which is mediated by high levels of circulating bradykinin). Side effects are rare and the drugs are usually well tolerated. Note: there are escape pathways in the formation of angiotensin II, such as CHYMASE enzyme, so the effect gets decreased over time. Every trial with ACE inhibitors shows benefit (improved survival, improved functional capacity) in patients with systolic HF.
Beta blockers
have been shown to improve outcomes in HF patients by INHIBITING CARDIOTOXIC EFFECTS OF CATECHOLAMINES that are elevated in patients with HF. They block the binding of norepinephrine and epinephrine to beta1 receptor in the myocardium, resulting in decreased heart rate and decreased neurohormonal activation. They lead to recovery of myocardial function. They are also anti-ischemic, anti-hypertensive, anti-arrhythmic, antioxidant, and anti-proliferative. Beta receptors also gradually lead to apoptosis in the myocardium (leading to worsening ventricular function), and beta blockers prevent this process and allow for cardiac recovery. INDICATIONS: symptomatic heart failure, asymptomatic ventricular dysfunction (LV EF<35-40%), and after MI. Trials have shown that there are improved outcomes with bta blockers compared to placebo (other standard therapies)
Shortcut method to determine if there is normal axis
if lead II has primarily positive deflection and lead aVF has primarily positive deflection, then it is normal axis.
Steady state HR
if the intensity of exercise remains constant, the HR will level off at a rate where the metabolic needs of the body can be met.
2nd degree SA block type 2
if the p-p interval is stable and the pause is a multiple of the p-p interval, it is type 2 2nd degree SA block. (don't think we need to know the SA blocks)
2nd degree SA block type 1
if there is a pause on a telemetry strip: measure the p-p intervals. If the p-p intervals are getting shorter before a pause, and the pause is not a multiple of the time between p-p, it is type 1 SA exit block. (don't think we need to know the SA blocks)
Acute management of polymorphic ventricular tachycardia if UNSTABLE.
if unstable, defibrillation, IV magnesium, and accelerate the heart rate (via ISOPROTERENOL [nonselective beta agonist] or overdrive pace (temporary pacemaker). Also, correct the underlying cause (correct electrolytes, stop offending medications). Note: the QT interval is dependent on the heart rate. The slower the heart rate, the longer the QT interval. The faster the heart rate, the shorter the QT interval. If patient is in an unstable rhythm due to Torsades (caused by long QT interval), the goal is to SHORTEN THE QT INTERVAL.
Aortic regurgitation/insufficiency
inability of AV leaflets to CLOSE FULLY, which results in backflow of blood from ascending aorta to LV during diastole. Etiology: Congenital aortic root dilation (Marfan syndrome, Ehler-Danlos syndrome), endocarditis, aortic dissection. History: EXERCISE INTOLERANCE, DYSPNEA, orthopnea, paroxysmal nocturnal dyspnea. Physical exam: signs of CHF, S2 is soft or loud, SOFT EARLY DIASTOLIC MURMUR, mid-diastolic murmur of functional MS (AUSTIN-FLINT MURMUR). Physical signs: Waterhammer (collapsing) pulse, Corrigan's sign, De Musset's sign, Duroziez's sign, Quincke's sign, Traube's sign, Muller's sign.
Mitral regurgitation
inability of mitral valve to CLOSE FULLY, which results in backflow of blood from LV to LA during SYSTOLE. Can be caused by multiple etiologies: MV prolapse, endocarditis, LV dysfunction/dilation, Rheumatic heart disease, congenital. Pathophysiology: MV fails to create a seal between the LV and LA. Blood regurgitates from the LV to the LA during systole, leading to LA VOLUME OVERLOAD. Blood then recirculates back into the LV during diastole, leading to LV VOLUME OVERLOAD. LA pressure is a function of both LA blood volume and LA stiffness. In normal patient, the LA is small and stiff. If there is acute MR: the LA is still small and stiff but the LA pressure is very high. The LV is relatively small because it hasn't been enlarged by chronic volume overload. The LA pressure is high enough to cause rapid pulmonary edema, which can be fatal without surgical correction. In chronic MR: the LA is compliant and large, and the LA pressure is either normal or high. The LV is ENLARGED. Patient may be asymptomatic for decades until LV dysfunction develops. Symptoms: determined by the degree of LA pressure rise, which is dependent on the regurgitant volume and LA stiffness. Symptoms are EXERCISE INTOLERANCE, DYSPNEA, ORTHOPNEA, PAROXYSMAL NOCTURNAL DYSPNEA. Physical exam: signs of CHF, S1 IS SOFT, S3 GALLOP, and HOLOSYSTOLIC MURMUR.
Aortic stenosis
inability of the Aortic valve to FULLY OPEN, resulting in impeded outflow from the LV to the ascending aorta during SYSTOLE. Etiology: Senile calcific AS (in elderly), congenital AV abnormalities (bicuspid AV is most common), and Rheumatic heart disease. Symptoms: triad of CHF, ANGINA, & SYNCOPE (or sudden death). Physical exam: signs of heart failure, S2 ABSENT (in severe AS), S4 GALLOP, HARSH LATE PEAKING SYSTOLIC CRESCENDO-DECRESCENDO MURMUR. Treatment: surgery is best option (replace valve with mechanical bileaflet, single leaflet, cow valve, pig valve, cadaver valve), or percutaneous TAVR if patient cannot get surgery
Chronotropic incompetence
inability to reach 85% of maximum predicted HR
Shock
inadequate oxygen delivery to meet metabolic demands. Results in GLOBAL TISSUE HYPOPERFUSION and METABOLIC ACIDOSIS. Shock can occur with a normal blood pressure, and hypotension can occur without shock. Pathophysiology: inadequate systemic oxygen delivery, activation of autonomic responses (epinephrine, norepinephrine, dopamine, & cortisol) in an attempt to maintain systemic oxygen delivery. These hormones (epinephrine, norepinephrine, dopamine, and cortisol) cause vasoconstriction, increased HR, increased cardiac contractility, and therefore increased cardiac output. Ultimate goal of the body's response to shock is to MAINTAIN CEREBRAL & CARDIAC PERFUSION. This is achieved by vasoconstriction of splanchnic, musculoskeletal, and renal blood flow. Physiologic effects of shock: cardiac depression (decreased or increased HR), respiratory distress (dyspnea, may require intubation), renal failure (anuria, elevated creatinine), disseminated intravascular coagulation, end organ failure.
Venous thromboembolic diseases
includes DVTs and PEs. PEs do not directly injure the right heart, but if there is an obstruction of the pulmonary artery, it puts increased pressure on the right ventricle. DVTs can embolize through the heart and into the right, left, or both pulmonary arteries. This increases pressure in the RV and causes right ventricular dilation and weakness.
Effects of exercise on the body
increased oxygen demand (HR and SV increase), metabolic speed increases (nutrients are used up (glycogen, glucose, amino acids). When stores get depleted, then proteins get consumed. More waste is produced (especially lactic acid)), and body temperature rises (hyperthermic state, particularly during prolonged exercise)
Exudate
inflammation (high levels of protein and WBCs). If it is exudative, it is much more likely to be bacterial in origin. Should be treated with antibiotics and surgical drainage.
Myocarditis
inflammation of the heart. It is a cause (NOT a response) to mycardial injury. Mostly caused by Coxsackieviruses A and B and other viruses (can also be idiopathic, fungal, bacterial, and others, but assume it is caused by a virus until proven otherwise). ACTIVE PHASE: heart may be normal or dilated, some hypertrophy may be present, and the lesions may be diffuse or patchy. The ventricular myocardium is typically flabby and mottled (pale foci/microabscesses or minute hemorrhagic lesions). Mural thrombi may be present in any chamber (because the heart is not working well). Histology: Interstitial INFLAMMATION (lymphocytic>neutrophils, because myocarditis is mostly caused by virus) and FOCAL NECROSIS OF MYOCYTES adjacent to the inflammatory cells. Note: myocarditis can also be caused by HYPERSENSITIVITY reaction (allergic), so there are lots of eosinophils and mononuclear inflammatory cells, predominantly localized to the perivascular and large interstitial spaces, but it is uncommon.
Myocarditis
inflammation of the myocardium. Symptoms: DYSPNEA (increased pressure within lung), CHEST PAIN (from acute inflammation of the chest), ARRHYTHMIAS (because inflammation interrupts the conduction center of the heart. Can occur in atria or ventricles), PUMP FAILURE (acute cardiogenic shock), EMBOLIC EVENTS, SUDDEN DEATH (most commonly caused by ventricular arrhythmias). Diagnosis: histopathology (Dallas criteria), Clinical (chest pain, severe hemodynamic compromise, advanced heart failure syndrome, ELEVATED TROPONIN/CARDIAC ENZYMES, EKG with ST elevations in non-coronary artery distributions, T wave inversions or Q waves despite normal or non-obstructive coronary arteries), or advanced cardiac imaging. Presentation is very similar to heart attack. However, when coronary angiogram is done it appears normal. Once MI is excluded, it is likely that patient has myocarditis. Etiology of myocarditis: viruses, bacteria, fungal. Almost any infectious, non-infectious, and medications (antibiotics, anti-convulsants, cardiac drugs, and others) can cause inflammation of the heart. direct cytotoxic effect of the causative agent leads to cell death, and then there is a secondary immune response which often makes things worse. Cytokines are expressed within the myocardium, and it can lead to aberrant induction of APOPTOSIS.
Pericarditis
inflammation of the pericardium. Can be acute, subacute, incessant, or recurrent. There are many different things that can cause pericarditis (viruses, bacteria, fungi, parasites, autoimmune, neoplastic, metabolic, trauma, drug-related, etc). Viral pericarditis is common, and bacterial pericarditis is uncommon but more catastrophic. Autoimmune pericarditis is fairly common, and uremia (from renal failure) is another common cause.
Nutrient-drug interactions: Warfarin
keep vitamin K intake consistent.
Global tissue hypoxia
leads to endothelial inflammation and disruption, and causes inability of oxygen delivery to meet demands of the organs. This results in LACTIC ACIDOSIS, CARDIOVASCULAR INSUFFICIENCY (heart is not contracting well so there is decreased cardiac output and decreased blood pressure), and INCREASED METABOLIC DEMANDS.
Inward rectifier potassium channel (I-K1)
maintains high K permeability during phase 4. its decay in the pacemaker potential contributes to diastolic depolarization. Voltage-gated.
Heart failure: prognosis
many different variables predict outcomes. LV ejection fraction is very important (lower ejection fraction results in higher mortality). Other predictors of mortality: circulating levels of NOREPINEPHRINE, ANGIOGENSIN II, ENDOTHELIN. Therapies cannot do much to improve ejection fraction. Current therapies focus on treating the other aspects of pathophysiology of heart failure. (Current therapies are focused on systolic heart failure, bc there aren't yet good therapies for diastolic heart failures).
Staph aureus
more likely to infect either healthy or deformed valves (10-20% of cases), particularly IV drug users
Streptococcus viridans
more likely to infect previously damaged or abnormal valves (50-60% of cases)
Dilated cardiomyopathy
most common form of cardiomyopathy. Poor contractility leads to increased end systolic volume and end diastolic volume. This leads to DILATION and heart failure. Etiologies: INFECTION (myocarditis), CARDIOTOXIC DRUGS/CHEMICALS (including ETOH, some chemotherapies), nutritional disorders, GENETICS (about 1/3 of cases), PREGNANCY (probably multifactorial), autoimmune, idiopathic. Clinical picture: slow onset of CHF, poor ejection fraction, mitral regurgitation, arrhythmias, embolism, and can have death within 5 years. Gross image: heavy, flabby heart with dilated chambers and thin walls. Because the heart is not contracting well, thrombi can form and cause ischemia in other parts of the body. Histology: demonstrates VARIABLE MYOCYTE HYPERTROPHY (with boxcar nuclei) and INTERSTITIAL FIBROSIS that goes around individual myocytes.
Ventricular arrhythmias
most commonly seen with structural heart disease (commonly prior MI with scar) and usually associated with systolic heart failure. can be lethal and lead to sudden death, especially in people with heart failure. 2 main types: Ventricular tachycardia and Ventricular fibrillation.
Type 4 AADs
nondihydropyridine calcium channel blockers
P wave
normally <2.5 boxes high and <3 boxes wide. It is best seen in leads II and V1. It is normally inverted in aVR. It is created from SA node firing and atrial capture. It may be absent in an arrhythmia such as atrial fibrillation. It may be larger/longer if there is left and/or right atrial enlargement.
Pericardial effusion
normally there is 10-50 mL fluid present between the visceral and parietal pericardium, which is made of plasma ultrafiltrate. During pericardial effusion, there is increased pericardial fluid. Characterized by onset (acute, subacute, chronic), size (mild <10 mm, moderate 10-20 mm, large>20 mm), distribution (circumferential or loculated [walled off on a certain area of the heart]), and by composition (transudate or exudate). it can lead to cardiac tamponade.
Neurogenic shock
occurs after acute spinal cord injury. The sympathetic outflow is disrupted, resulting in unopposed vagal tone. This results in hypotension and bradycardia. Treatment: ABCs, remember cervical spine precautions (cervical collar), Fluid resuscitation (MAP >85-90 mmHg for first 7 days, which is thought to minimize secondary cord injury). If crystalloid is insufficient, use vasopressors. Search for other causes of hypotension. For bradycardia, give Atropine and/or temporary pacemaker.
S4 heart sound
occurs during phase 1 (atrial contraction). It is caused by vibrations of the ventricular wall with ventricular filling. It is usually associated with disorders such as cardiac hypertrophy and a stiffer than normal ventricle.
S3 heart sound
occurs during phase 6 (rapid filling phase). It results from the rapid flow of blood from the atria to the ventricles. It is typically not audible in normal adults, but it is often heard in children and athletes. It can also occur during certain pathological processes.
Aortic stenosis
occurs when the aortic valve does not open completely, due to a narrowed valve opening which occurs during ventricular systole. As a result, less blood can be ejected from the LV to the aorta. You can hear a MID-SYSTOLIC crescendo-decrescendo MURMUR and an EJECTION SOUND (due to mobile aortic valve leaflets). Can be due to a congenital abnormality (bicuspid aortic valve, which causes aortic stenosis later in life) or an acquired abnormality (due to calcifications which occur with aging, which is quite common). As a result of AS, there is a LARGE PRESSURE GRADIENT between the LV pressure and Aortic pressure during systole (LV>>Aortic pressure), due to the narrowed valve which causes a significantly higher afterload for the left ventricle. There is also INCREASED END SYSTOLIC VOLUME (ESV) and REDUCED STROKE VOLUME. Left ventricular hypertrophy, myocardial dysfunction, arrhythmias, and left heart failure may occur over time. PV loop also shows increase in LV pressure and significant increase in end systolic volume.
Aortic regurgitation/insufficiency
occurs when the aortic valve is leaky, causing backflow of blood into the LV. It can result from several pathological mechanisms caused by connective tissue defects (Marfan syndrome and Ehler-Danlos syndrome), endocarditis (from bacterial infections. With AR, there is backflow of blood from aorta into LV during diastole. AR produce a DESCENDING DIASTOLIC MURMUR. AR results in LV VOLUME OVERLOAD (due to backflow of blood from aorta to LV) and SHARPLY INCREASED LV END DIASTOLIC PRESSURE (shifts the PV loop to much higher pressure). The blood volume is ejected into the aorta, but some blood flows back into the LV during filling. This can lead to reduced diastolic pressure in the aorta. There is elevated systolic pressure and decreased diastolic pressure, resulting in WIDENED PULSE PRESSURE. Decreased blood flow into the arterial circulation and body systems can also occur over time. On the PV loop, the isovolumic phases are lost and there is a significant increase in the EDV. There is also a slight increase in systolic pressure during ejection.
Mitral stenosis
occurs when the mitral valve does not open completely. Results in a MID DIASTOLIC HEART MURMUR due to the high resistance of blood flow from the atria to the ventricles and the elevated LA-LV pressure gradient. There can also be an OPENING SNAP MURMUR (due to the mitral valve opening slightly earlier than normal due to the elevated LA pressure). Mitral stenosis is usually an acquired abnormality (from RHEUMATIC FEVER, but usually develops later in life, 20+ years after the onset of rheumatic fever). There is increased blood volume in the LA, elevated LA pressure, atrial hypertrophy, atrial dilation, and reduced LV filling (resulting in decreased EDV and stroke volume). Atrial enlargement may cause abnormal electrical activity and ATRIAL FIBRILLATION. Elevated LA pressure may lead to increased pressure in pulmonary vessels (pulmonary HTN, pulmonary edema, and eventually R heart failure). On Wiggers diagram: elevated LA volume and LA pressure leads to a gradient between LA and LV. On P-V loop: less blood can move into the LV, so EDV and stroke volume are decreased, and ESV is also reduced slightly because ventricular filling is reduced.
Mitral regurgitation/insufficiency
occurs when the mitral valve is leaky, causing a backflow of blood from the LV to the LA during systole. It can occur due to acute cardiovascular changes (rupture of the chordae tentineae with MI), chronic cardiovascular changes (ischemic cardiomyopathy or Mitral valve prolapse). It results in a HOLOSYSTOLIC MURMUR throughout the entire duration of systole (due to the backward flow of blood into the LA from LV, which is best heard over the LV), and also an S3 SOUND (during the rapid filling phase of ventricular diastole, when 2/3 of blood is moving into the LV). Wiggers diagram shows that there is a REGURGITANT JET of blood flowing into the LA during systole , which causes volume overload of the LA during systole. As a result there is increased LA pressure which peaks toward the end of systole, resulting in a TALLER V WAVE on the LA pressure curve. LA pressure peaks at the time of S2. the sudden rise in LA pressures produces increased pulmonary pressures, resulting in PULMONARY EDEMA. With chronic MR, LV hypertrophy and dilation can occur (due to increased EDV). P-V loop for chronic MR shows significant increase in LV volume, loss of isovolumic phases (because the mitral valve does not close completely, resulting in continuous movement of blood)
Eosinophilic myocarditis
often MEDICATION-INDUCED (non-infectious). Usually seen in older patients (mean age 58). Symptoms: rash/urticaria, fever, EKG abnormalities. Important to diagnose correctly because it is readily treatable with HIGH DOSE STEROIDS + AZATHIOPRINE.
Gap junctions
part of the intercalated disc that allows for the transfer of electrical activity/ions between cells. The presence of gap junctions between cardiac myocytes allows a flow of current from the depolarized cell to a neighboring cell that has not been electrically stimulated. Once ion movement depolarizes the cell membrane of the neighboring cell, an action potential will be elicited in this cell.
Desmosome
part of the intercalated disc that allows for the transfer of force between cells
Definite infectious endocarditis
pathology (biopsy-this is not done much because it really damages the valve), clinical (2 major, 1 major+3minor, or 5 minor)
Lymphocytic myocarditis
pathophysiology is not well understood. Mean age is 43 years. Treatment: corticosteroids and immunosuppressive drugs (controversial)
Septic shock
patient meets at least 2 SIRS criteria: patient is febrile (>38) or hypothermic (<36), HR>90, RR>20, WBCs >12000 (leukocytosis) or <4000 (leukopenic) with the presumed existence of infection. Blood pressure can be "normal." Clinical signs: hyper- or hypothermia, tachycardia, low BP (SBP<90), mental status changes. Management: 2 large bore IV with NS bolus, supplemental oxygen, EMPIRIC ANTIBIOTICS based on suspected source ASAP after blood culture. If patient has persistent hypotension despite giving antibiotics and IV fluids, give vasopressors (norepinephrine, dopamine, etc) and titrate to achieve MAP>60. Studies: cardiac monitor, pulse oximetry, labs (CBC, chem7, coagulation studies, LFTs, lipase, UA, ABG with lactate), blood culture x2, urine culture, CXR.
Incessant pericarditis
pericarditis lasting >4-6 weeks but <3 months without remission
Chronic pericarditis
pericarditis lasting for >3 months
Type 3 AADs
potassium channel blockers
Nitrates/Hydralazine
potent vasodilators. In certain patients with HF, there is reduced amounts of NO, so Nitrates and Hydralazine augment NO availability. FDA has approved Isorbide ninitrate+Hydralazine be given for treatment for HF in African Americans. There is ongoing interest in repeating the trial across patient populations.
Nonbacterial thrombotic endocarditis/Marantic endocarditis
predisposing conditions: debilitations (due to cancer, sepsis, etc), systemic HYPERCOAGULABLE state, TROUSSEAU SYNDROME of migratory thrombophlebitis (associated with pancreatic and lung cancer), ENDOCARDIAL TRAUMA (indwelling catheters, SWAN-GANZ pulmonary artery catheters). Gross image: larger fibrinous sterile vegetations along the lines of closure of the valve cusps. 1-5 mm, can be single or multiple. Histology: FIBRIN THROMBI are loosely attached to the underlying valve. The vegetations are NOT INVASIVE and there is no inflammation. Can cause SYSTEMIC EMBOLI and produce infarcts in the brain, heart, or elsewhere.
Chronic active myocarditis & Chronic persistant myocarditis:
presents as heart failure with PERSISTENT lymphocytic cellular infiltrate. It persists because we do not have direct therapies for this. With chronic active and chronic persistent myocarditis, the lymphocytic infiltrate never fully resolves, and pump function gradually decreases over months and years, so long-term mortality is lower.
Acute myocarditis
presents as heart failure with reduced EF but near normal LV dilation, but not as severe as fulminant myocarditis. With acute myocarditis, the lymphocytic infiltrate never fully resolves, and pump function gradually decreases over months and years, so long-term mortality is lower.
Colchicine
prevents microtubule polymerization, and prevents neutrophils from getting into the pericardium. It has been shown to decrease events and rates of recurrence.
Angiotensin receptor (AT1) blockers
prevents the effects of Angiotensin II (whether it was made by ACE, chymase, or other escape pathways. They are not quite as effective as ACE inhibitors (probably because ACE inhibitors have dual effect of blocking formation of Angiotensin II and increasing circulating levels of bradykinin). Note: over time, ACE inhibitors are a bit better than ARBs, which is why ACE inhibitors are the first line therapy.
Distributive shock (septic/neurogenic)
principle hemodynamic compromise is DECREASED AFTERLOAD/SYSTEMIC VASCULAR RESISTANCE due to profound vasodilation. Venous return is also reduced. Cardiac output increases to try to compensate. Mixed venous oxygen saturation is high. Treatment: alpha1 agonists to increase SVR (pressors), IV fluids.
Cardiogenic shock
principle hemodynamic compromise is DECREASED CARDIAC OUTPUT. Arterioles constrict to increase SVR and increase afterload, and there is also increased preload (you would see JVD). Etiology: acute MI, myocarditis, myocardial contusion, aortic stenosis, mitral stenosis, hypertrophic cardiomyopathy, acute aortic insufficiency. Defined as SBP <90 mmHg, cardiac index <2.2 L/min/m2 body surface area, and pulmonary capillary wedge pressure >18 mmHg. Signs: cool/clammy skin, shortness of breath, tachypnea, hypotension, altered mental status, narrowed pulse pressure, and may see rales/murmur. Mixed venous oxygen saturation is also low. Pathophysiology: when there is 40% loss of LV function after ischemia, patients can present with cardiogenic shock, due to reduced cardiac output, there is LACTIC ACIDOSIS and hypoxia. Stroke volume is reduced, so there is TACHYCARDIA to compensate, which worsens the ischemia and infarction. Tests: EKG, CXR< labs, cardiac enzymes, coagulation studies, echo, cardiac monitor, pulse oximetry. Management: ABCs, give oxygen, intubate if needed, ASPIRIN (4 chewable), beta blocker, morphine, Heparin, treat the MI via revascularization, mechanical assist device, etc. Note: For RV infarct: don't give nitroglycerin!! It decreases blood pressure, reduces preload, and it would be harmful. Give IV fluid to increase venous return to right heart, and give inotrope to increase contractility. For acute mitral regurgitation or VSD, treat with pressors (Dobutamine and Nitroprusside)
Hypovolemic shock
principle hemodynamic compromise is DECREASED PRELOAD. To compensate, cardiac output (heart rate and contractility increase), and SVR increases (because most arterioles constrict to redistribute blood to other parts of the body). Mixed venous oxygen saturation is also low. Causes of hypovolemic shock: vomiting, diarrhea, bowel obstruction, pancreatitis, high degree burns, neglect, dehydration, GI bleed (including melanotic stools), trauma, massive hemoptysis, AAA rupture, aortic dissection, ectopic pregnancy, post-partum bleeding. Management: ABCs, 2 large bore IVs or central line, GIVE FLUIDS (NS, LR, PRBCs). Control any bleeding. arrange definitive treatment of underlying cause. Labs: CBC, ABG, lactate, electrolytes, BUN/creatinine, coagulation studies, type and cross match (for future blood transfusion). Other diagnostics: CXR, pelvic xray, CT abdomen/pelvis, Chest CT, GI endoscopy, bronchoscopy, vascular radiology
Arrhythmogenic (right) ventricular cardiomyopathy
progressive fibro-fatty replacement of the right (and sometimes also left) ventricle. Due to mutation (either inherited or spontaneous mutation).
Synchronized cardioversion
put pads on patient. The little dots above QRS mean that the machine will synchronize with the heart rhythm and DELIVER SHOCK DURING R WAVE.
Pericardiocentesis
putting a needle through the chest into the pericardial space and aspirating the pericardial effusion fluid. As fluid is aspirated, the heart is able to decompress and fill. When intrapericardial pressure < RA pressure, the heart can re-fill with blood. This is the first treatment of cardiac tamponade. The fluid from the effusion can be sent for analysis.
Recurrent pericarditis
recurrence of pericarditis after a documented first episode of acute pericarditis, total remission of symptoms for 4-6 weeks, and then the pericarditis comes back
Diet for CHF
reducing dietary sodium (<2000 mg) helps reduce strain on the heart in patient with CHF. Fluid restriction may be indicated for CHF patients with signs of fluid overload. PATIENT EDUCATION is important for the efficacy of complying with CHF dietary recommendations.
Treatment of regurgitant valves
regurgitant valves may be treated even before they become symptomatic to preserve LV function (and prevent remodeling of the left ventricle).
Q wave
represents the left→right depolarization of the interventricular septum. Small septal Q waves are typically seen in the left sided leads (1, aVL, V5, V6). Small Q waves are normal in most leads, but they can be abnormal (can be abnormally large due to a scar such as old MI). ABNORMAL Q wave: Q wave is abnormal if it is wider than 1 small box, >2 mm deep, >25% the depth of the QRS, or if it is seen in leads V1-V3
End diastolic pressure-volume relationship (EDPVR)
represents the passive filling curve for the left ventricle. Passive forces are greater in cardiac muscle than skeletal muscle, because as you increase the stretch on the muscle wall itself, there is greater passive tension that develops in cardiac muscle. EDPVR also represents the ELASTANCE of the left ventricle (∆P/∆V) [the inverse of compliance]. Note: it is the curved line that contains the P-V loop.
Potassium channel (acetylcholine activated) (I-K/ACh)
responsible for effects of enhanced vagal stimulation. Decreases diastolic depolarization (and HR) with parasympathetic stimulation, and hyperpolarizes the resting membrane potential. Ligand (ACh) gated.
Restrictive cardiomyopathy
restricted filling and reduced diastolic size of either one or both ventricles due to impairment in relaxation (from causes that result from infiltration of the heart muscle by proteins such as sarcoidosis or amyloidosis). Systolic function may be normal or near-normal (though can progress to severe systolic dysfunction). Can be idiopathic or associated with other diseases such as AMYLOID which causes an infiltrative restrictive cardiomyopathy.
Cor pulmonale
right sided heart failure due to pulmonary hypertension. Pulmonary edema is not prominent
Pulmonary arterial hypertension (group 1 PA)
risk factors include collagen vascular disease, congenital heart disease, portal hypertension, HIV infection, drugs/toxins (weight loss drugs, methamphetamines, cocaine), pregnancy. These risk factors in certain susceptible hosts sustain vascular injury, which leads to decreased NO and prostacyclin (vasodilators) synthesis and increased Thromboxane and endothelin (vasoconstrictors) synthesis, leading to constriction of vessels. This also leads to release of growth factors secreted in the lung, which cause the development of PLEXIFORM LESIONS within the lung (smooth muscle cell proliferation within the arterial wall which constricts the bloodflow). Symptoms: nonspecific (dyspnea, weakness, recurrent syncope, fatigue, angina, palpitations, and abdominal distension. Usually initial symptoms are provoked by exertion, but ultimately symptoms may occur at rest). Physical exam: left parasternal left (RV dilation), loud P2 component of S2, pansystolic murmur of tricuspid regurgitation, diastolic murmur of pulmonic insufficiency, S3 gallop, JVD, hepatomegaly, edema, ascites, cyanoss, cool extremities. lung exam is usually normal. Diagnosis: by clinical suspicion, echo, and right heart catheterization.
Wandering atrial pacemaker
same as multifocal atrial tachycardia except the HR<100.
Monomorphic ventricular tachycardia
same morphology throughout. QRS is wide, rate >100 BPM, and ventricular contractions are more frequent than atrial contractions. It is usually due to STRUCTURAL HEART DISEASE (especially prior MI with scar [which does not conduct, but a circuit can form around the scar] or systolic heart failure) and REENTRY.
Anaphylactic shock
severe systemic hypersensitivity reaction characterized by multisystem involvement and it is IgE mediated. Symptoms: first there is pruritis, flushing, urticaria. Then there is throat fullness, anxiety, chest tightness, shortness of breath, & lightheadedness. Then there can be altered mental status, respiratory distress, and circulatory collapse. Clinical symptoms: airway compromise, hypotension, and/or involvement of cutaneous, respiratory, or GI symptoms. Look for exposure to drug, food, or insect. Treatment: maintain/protect airway, breathing, & circulation. May require immediate intubation due to angioedema and/or respiratory compromise. Put on cardiac monitor and pulse oximetry monitor. Give IV fluids, oxygen, and EPINEPHRINE 0.3 mg IM (every 5-10 mins as needed). Second line drug: corticosteroids, H1/H2 blockers.
PR interval
should be 120-200 ms (.12-.2 s aka 3-5 small boxes). It represents the sinus node firing and the impulse arrives at the ventricles. Long PR interval (>200 ms) is caused by slow conduction or block from atrium to ventricles (1st and 2nd degree heart block). Short PR interval (<120 ms) Caused by conduction from atrium to ventricle via a bypass tract.
Wiggers diagram
shows many different events that recorded throughout one phase of systole and one phase of diastole. These events are recorded using pressure transducers (left atrial pressure, ventricular pressure, aortic pressure, and venous pulse pressure), phonocardiogram (heart sounds), EKG, and ventricular volumes.
venous function curve
shows the relationship between venous return and central venous pressure (aka RA pressure). As central venous pressure is increasing, the venous return is decreasing. There is an inverse relationship between central venous pressure and venous return. Normal RA pressure is 2 mmHg (corresponding with venous return aka cardiac output of about 5 L/min). Note: when central venous pressure <0 mmHg, there is a plateau in venous return. That is because intrathoracic pressure is ~0 mmHg. When central venous pressure is <0 mmHg, there is compression of the great vessels in the central venous compartment, so the venous return cannot increase further.
Goals for antiarrhythmatic drugs
slow conduction velocity (to disrupt the circuit) and prolong the refractory period to get rid of the excitable gap. Note: AADs may be arrhythmogenic because they may cause an arrhythmia by altering conduction velocity and refractory period.
Endocarditis of SLE aka Libman-Sacks Endocarditis
small sterile vegetations that are seen along the undersurfaces of the AV valves, endocardium, and chordae. Affects the MITRAL AND TRICUSPID VALVES. Histology: fibrinous vegetations, often with NECROSIS of the underlying valve. Vegetations involving the surface and/or undersurface of the valves. HEMATOXYLIN BODIES (degenerated nuclei that have been attacked by anti-nuclear antibody) may be seen. FIBROSIS AND DEFORMITIES CAN RESEMBLE CHRONIC RHEUMATIC HEART DISEASE and require surgery.
Type 1A, 1B, 1C AADs
sodium channel blockers
Sodium channel blockers
sodium channels are responsible for phase 0, and they are the predominant current in His/Purkinje tissue (not nodal tissue). Overall effect of sodium channel blockers is DECREASED CONDUCTION VELOCITY by altering the slope of phase 0 (making it less steep).
sodium recommendations for people with heart failure and HTN
sodium intake <1800 mg/day
Venousthromboembolism: treatment
start Warfarin (vitamin K antagonist) IV ASAP. Can also use heparin, low molecular weight heparin, or Fondaparinux. NOAC (aka DOAC-direct oral anticoagulant) may be safer than Heparin/Coumadin. Provide HEMODYNAMIC SUPPORT (Norepinephrine, Dobutamine/Dopamine, Epinephrine-best option). If patient has PE with shock, treat with IV fibrinolytic therapy (make sure patient doesn't have contraindications). Surgical interventions: Catheter in pulmonary vessels to extract the thrombus or break it into smaller fragments, or take patient to OR and open pulmonary arteries to suck clot out if it is too big.
Treatment of stenotic valves
stenotic valves are generally not treated unless they are symptomatic. In general, valvular lesions are NOT symptomatic unless they are SEVERE.
Venousthromboembolism: predisposing factors
surgery, cancer (especially heme, lung, GI pancreatic, brain), trauma, immobilization, pregnancy or recent delivery, oral contraceptive pills, hormone replacement, atherosclerotic risk factors (HTN, DM, HLD), hospitalizations. However, about 30% are "unprovoked" (causative factors are unknown, so it is harder to prevent future VTEs).
Rheumatic heart disease
symptoms are MIGRATORY POLYARTHRITIS, POLYCARDITIS, (lesions at all levels of the heart), SUBCUTANEOUS NODULES, ERYTHEMA MARGINATUM, and SYDENHAM CHOREA (jerking movements of hands, face, etc). Gross image: the valve becomes very scarred and the leaflets are thickened. The MITRAL VALVE is virtually always involved. Gross findings: thickened leaflets, COMMISURES ARE FUSED. The chordae become fused, thickened, and shortened. Histology: organization of acute inflammation, diffuse fibrosis and neovascularization, obliteration of leaflet architecture.
Bruce protocol for treadmill test
systematic approach. Every 3 minutes there is an increase in the rate and grade of exercise. It gives the body time to adapt and it then keeps getting faster. During exercise stress test (Bruce protocol), the goal is to achieve 85% of the maximum predicted HR.
AV nodal blocker
terminates the AV nodal dependent tachycardia by terminating the reentry circuit. Treatment options: carotid sinus massage, adenosine, Beta blockers (IV), Calcium channel blockers (IV), and Digoxin (not commonly used)
Giant cell myocarditis
the #1 cause of fulminant myocarditis, and prognosis is poor. Mean age affected is 53 years. There is progressive LV dilation and arrhythmias. Treatment: early transplant evaluation + immunosuppressive therapy. Advanced heart failure therapies such as Ventricular assist devices (battery operated & permanent or until transplant), VV and VA ECMO (circulates blood from venous circulation through an oxygenator) can be used too. Histology: myocytes degenerate and there are multi-nucleate giant cells along with inflammatory cells.
Calcific aortic stenosis
the MOST COMMON of all valvular abnormalities. Seen in old people (age 70-90), and seen younger (age 50-70) in people born with a bicuspid aortic valve. It is caused by WEAR AND TEAR DEGENERATION causing dystrophic and passive ACCUMULATION OF CALCIUM SALT HYDROXYAPATITE, which injures the endothelial cells and causes secondary degenerative changes. More common in people with HTN, HLD, and inflammation. The valve injury is different from the valve injury caused by atherosclerosis. Gross image shows calcified masses on the cusps which prevent opening. the Commissures (cusps) are usually NOT FUSED. Histology: fibrosis, calcification, lipid deposits. Note: with calcific AS, there is gradual narrowing of the valve orifice, so as a result, concentric LV hypertrophy can develop due to the increasing pressure gradient. The hypertrophied myocardium tends to be ischemic and not able to contract as well. Symptoms develop when there is DECOMPENSATION. Without valve replacement, 50% with angina die within 5 years, and 50% with CHF die within 2 years.
Pacemaker myocytes: action potential
the SA and AV nodal cells, about 5% of cardiac cells. Lowest membrane potential is about -60 mV. Phase 4=slow depolarization (pacemaker potential, due to opening of FUNNY CHANNELS, inward-rectifying potassium channels, T type calcium channels, and L-type calcium channels. there is spontanious depolarizatios until the threshold of ~-40 mV is reached). Phase 0=depolarization phase (due to voltage-gated L-type CALCIUM channels). Phase 3=repolarization phase (due to delayed-rectifier potassium channels). Note: phases 1 and 2 do not exist in pacemaker action potentials. Action potential in pacemaker cells last ~150 ms.
SA node
the SA node is surrounded by perinodal tissue on the right atrium. When the SA node fires, it sends impulses through the perinodal tissue and it gets captured in the atrium, causing a P wave on EKG. Disease of the SA node occurs if the SA node does not fire or the SA node fires but the electrical impulses cannot get through the perinodal tissue.
Excitability (responsiveness)
the ability of cardiac cells to respond to electrical activity. It affects to the REFRACTORY PERIOD (which is critical to normal electrical activity and normal heart function)
Conductivity
the ability of the heart to conduct the action potential from site of origin to all cardiac cells. It is determined by CARDIAC MUSCLE ANATOMY and the functional syncytium.
Automaticity
the ability of the heart to spontaneously fire action potentials. It is due to the PACEMAKER CELLS of the heart.
End systolic pressure-volume relationship (ESPVR)
the active tension curve for contractile force developed during ventricular contraction. It is associated with the myofilaments and calcium levels. Changes in active tension (such as sarcomere stretch) change this curve. Note: It is the straight line that contains the P-V loop.
Contractile myocyte: action potential
the atrial and ventricular muscle cells, which is about 95% of cardiac cells. Resting membrane potential is about -85 to -90 mV. Phase 0=RAPID depolarization (caused by opening of voltage-gated sodium channels). Phase 1=transient early repolarization (voltage gated sodium channels close and transient outward potassium channels open [Ito]). Phase 2=plateau phase (balance between L-type calcium channels and delayed-rectifying calcium channels). Phase 3=repolarization (caused by opening the rest of the delayed rectifier potassium channels). Phase 4=resting membrane potential (due to opening of inward-rectifying potassium channels and sodium leak channels). Action potential in contractile cells is ~250 ms.
Supranormal phase
the cell is transiently hyperexcitable and can fire a normal action potential. It occurs at the very end of phase 3 (because all of the ion channels have recovered but the membrane potential is slightly higher than resting membrane potential of -85 mV)
Absolute refractory period (ARP)
the cell is unable to fire an action potential (regardless of the size of the stimulus)
QTc interval
the corrected QT interval for heart rate. Normal range: 360-440 ms. Both long and short QT intervals are associated with malignant ventricular arrhythmias and are associated with sudden cardiac death.
Congestive heart failure
the inability to deliver what is needed to the organs, resulting in congestion of the organs. It is usually chronic but can be acute (after fluid overload, MI, acute valvular dysfunction, etc) but it is generally considered chronic. CHF is characterized by DIMINISHED CARDIAC OUTPUT (aka SYSTOLIC DYSFUNCTION) or damming back of blood in the venous system (DIASTOLIC FAILURE WITH INSUFFICIENT FILLING OF THE HEART), or both. CHF if NOT a disease, it is the end stage of many processes. May be left sided, right sided, or both. Degree of dysfunction and whether there is compensation is best evaluated outside the heart. Initially, the heart can compensate by release of CATECHOLAMINES and MYOCYTE HYPERTROPHY (due to adaptive molecular and cellular remodeling). This enlargement is later pathologic, with ineffective function/structure, and may cause arrhythmias. Later, when compensation fails, there is DILATION. Heart failure is an end stage of different processes (hypertension, valvular disease, MI). These cause increased cardiac work, leading to hypertrophy and/or dilation and eventually cardiac dysfunction. Histology: shows myocyte hypertrophy & BOXCAR NUCLEI (rectangular nuclei)
Preload
the initial stretching of a single cardiac myocyte prior to contraction. The stretching force that sets the muscle length just prior to the onset of contraction. In the heart, preload is the PASSIVE DISTENSION (stretch) of the LV at the end of its filling period, determined by the EDV (which is determined by venous return). Each ventricular contraction is to maintain the following relationship: Venous return=cardiac output. Changes in the resting sarcomere length affects the tension that the muscle is able to develop. The heart at rest does not operate at the optimal resting length, it operates at a resting length a bit lower. The heart is able to generate muscle tension based on the stretch that is placed on the muscle, and when the heart has to enhance its function, having an increase in the muscle length at rest enhances cardiac function. Note: when end diastolic pressure/volume increases, the preload increases.
Contractility aka inotropy
the intrinsic ability of the heart to contract independent of preload and afterload. Inotrophy refers to the level of calcium in the cytoplasm of the muscle cell. Changes in contractility can result from changes in the inotropic state (amount of intracellular calcium released from SR), changes in cardiac performance by contractile proteins (increasing/decreasing the # of sarcomeres), changing intracellular calcium concentration during excitation-contraction coupling, and presence of positive/negative inotropic agents. Recall: the ESPVR line varies with changes in inotropy. when inotropy is increased, the line is steeper, so ESV is decreased and stroke volume is increased.
Mitral stenosis
the mitral valve is unable to FULLY OPEN, so there is impeded flow from the LA to LV during DIASTOLE. Can be caused by RHEUMATIC HEART DISEASE (90% of cases), mitral annular calcification (MAC), or MV obstruction due to tumor (LEFT ATRIAL MYXOMA, a benign tumor of the heart that attaches to the interatrial atrium septum and fills the left atrium), thrombus (could be caused by mechanical valve), or membrane. there is progressive INCREASE in LA pressure and size. The LA can become so large that there is stagnation of blood in the LA, which can cause blood clots. Diagnosis: based on history (EXERCISE INTOLERANCE, DYSPNEA, orthopnea, paroxysmal nocturnal dyspnea), physical exam (signs of CHF, auscultation reveals LOUD S1, OPENING SNAP, and DIASTOLIC RUMBLE), and echo (diagnostic modality of choice, can see the orifice area, transmitral pressure gradient, and LA size). EKG is nonspecific, but could show P wave that is negative in V1 and large. Treatment: Balloon valvuloplasty, which increases the size of the orifice and delays the need for valve replacement.
Fulminant myocarditis
the most acute form. Patients present with shock, heart failure, and rhythm disturbances. These patients often require advance therapies (pump/partial circulatory devices/ventricular assist device/transplant). With Fulminant myocarditis, the patient is very sick. However, if the patient survives the first 2 weeks, then the heart completely heals and prognosis is excellent.
AV nodal reentry tachycardia
the most common AV nodal dependent tachycardia. There is a bimodal age distribution (more common in kids-teens and around age 55). There is conduction from A→V through a fast pathway and then conduction that spins around and conducts V→A. this sets up an electrical circuit that spins around the AV node. This is AV nodal reentry tachycardia.
SA node
the normal pacemaker of the heart. AP firing rate is 60-100 (including autonomic regulation). In the resting heart, there is a high degree of vagal tone at the SA node, which slows the resting heart rate.
Advanced second degree AV block
the p-p interval is regular, and there is grouped beating. The patient has 2+ consecutive p waves that are not conducted.
Third degree AV block aka complete AV block
the p-p interval is regular, the QRS-QRS interval is regular (but SLOW), but the p waves and QRS waves are UNRELATED and INDEPENDENT. This can occur at any anatomic level, but it is usually in the His or below. The ventricles are escaping at the fastest location (steepest phase 4 slope) that is firing from the bundle of His or lower. The lower in the ventricle, the flatter the phase 4 slope, so the slower the escape rate will be.
Cardiac conduction system
the pathway that allows electrical current to be conducted from the SA node to the various chambers of the heart. The cardiac conduction system is a very efficient route for cardiac conduction to move through the heart. Impulse route: SA node→internodal pathways to right atria & Bachmann's bundle to left atrium→AV node→Bundle of His→L & R bundle branches→Purkinje fibers→complete depolarization of the muscle (from apex toward base). Note: conduction through the AV node is the slowest (0.5 m/s), and conduction through the Purkinje fibers have the fastest conduction (4 m/s).
Pericardial constriction
the pericardium becomes rigid and hard, so it prevents the RA/RV from dilating and accepting bloodflow. With inspiration, the pericardium is not able to move to have a more negative pressure, so during inspiration, the pressure gradient limits bloodflow that can move through the lungs and be received by the LA. As a result, cardiac output decreases and blood pressure drops. Physical exam shows TACHYCARDIA, tachypnea, pulsus paradoxus, JVD, sometimes decreased breath sounds at bilateral bases, S3 gallop, pericardial knock, hepatomegaly, ascites, and lower extremity edema. CXR can show calcifications on the pericardium. There is chronic inflammation & thickening that occurs (commonly due to tuberculosis). Diagnosis is based on clinical suspicion + echo (gold standard for 1st line testing), CT, MRI, and/or cardiac catheterization. Treatment: empiric anti-inflammatory therapy, specific medical therapy if caused by infectious origin (tuberculosis, other bacteria). Mainstay of treatment of chronic permanent pericardial constriction is PERICARDIECTOMY. Constrictive pericarditis can follow any pericardial process, especially pericarditis. The risk of progression from pericarditis→restrictive pericarditis is low (<1%) for idiopathic/viral causes, intermediate (2-5%) for immune-mediated/neoplastic causes, and high (20-30%) for bacterial causes.
Afterload
the resistance to ejection of blood by the arterial system. It describes factors which impede the ejection of blood from the ventricles. When afterload is increased, the LV has to work much harder to pump the same volume of blood, and the end systolic volume is increased. Factors that affect afterload: volume of blood in arterial circulation, pressure in the aorta at the onset of ejection (due to hypertension, obstruction, etc), compliance of the aorta, and size of the aortic valve (such as aortic stenosis). when afterload is increased, the pressure against which the ventricle contracts is much greater, and the ESV will be higher. PV loop shows rise in LV pressure associated with the larger ventricular afterload. As a result of increased afterload, the curve intersects with the ESPVR line at a higher level, so the ESV is greater. Stroke volume is decreased. If increased afterload is persistent, the heart compensates by increasing the EDV to maintain normal stroke volume.
Functional refractory period
the time for the ion channels to recover from activation before the next stimulus can trigger an action potential. This refractory period prevents tetanic contraction of the cardiac muscle. It has 3 phases: Absolute refractory period, relative refractory period, and supranormal phase.
Factors that affect the clinical consequences of valvular heart disease
the valve involved, the degree of impairment, rate of development, and the rate/quality of compensatory mechanisms.
Ventricular tachycardia
the ventricles are contracting without atrial contraction, and the ventricles can contract independently of each other, which can cause hemodynamic compromise and sudden death. If there are ≥3 CONSECUTIVE PREMATURE BEATS FROM THE VENTRICLE, it is defined as ventricular tachycardia.
Mean systemic filling (circulatory filling) pressure
the volume of blood in the total systemic circuit, when the heart is in cardiac arrest and no blood is flowing through the system. If venous return=0, the mean systemic pressure is 7 mmHg. It is the pressure that is exerted on the walls of the vasculature from the blood volume that is present. It is altered by increasing or decreasing the total volume in the system.
Electrical cardioversion
the way to restore a normal rhythm in any unstable patient with a fast heart rate. Electrical cardioversion can also be done ELECTIVELY (if people do not tolerate atrial fibrillation/flutter).
Atrial and ventricular pacing
there are 2 sharp spikes: atrial pacing spikes (with P wave) and ventricular pacing spikes (with wide QRS).
Atrial fibrillation
there are NO ORGANIZED P WAVES, and there is an IRREGULARLY IRREGULAR R-R interval. Mechanism is unknown. The atrium has chaotic electrical activity, and it sends 400 impulses per minute to the AV node.
Atrial flutter
there are PROMINENT F (flutter) WAVES in a sawtooth pattern. The flutter waves are organized. The R-R interval is generally considered regular (but it can be irregular). The flutter waves march through the QRS and T waves, and sometimes distort them. Mechanism: there is an electrical circuit that spins around the atrium at about 300/minute in the atrium. Only about 1/3-4 of those get through to the ventricle. It is a MACRO-REENTRY CIRCUIT. Treatment: ablation to terminate the reentry circuit in the right atrium.
Multifocal atrial tachycardia (MAT)
there are at least 3 DIFFERENT P WAVE MORPHOLOGIES. There is an IRREGULARLY IRREGULAR ventricular response. Heart rate >100 bpm. It is a SECONDARY ELECTRICAL RESPONSE TO HYPOXIA. It usually resolves by giving the patient oxygen.
Mean electrical vector
there are lots of vectors that represent the depolarization as it occurs in different parts of the heart. The mean electrical vector estimates the sum of all the electrical vectors created as the ventricles depolarize. It normally moves from right to left and superior to inferior.
Second degree AV block type 2 aka Mobitz 2
there is a P wave without a QRS following it. Measure the p-p interval and it should be regular, but not every P wave causes a QRS (there is grouped beating). The PR interval before and after the skipped QRS is the same, so it is a 2nd degree AV block type 2 aka Mobitz 2. Note: the QRS is usually wide compared to normal - sometimes this can be a clue of disease below the AV node (in the His or below). If patient has this: there is a high rate of progression to complete heart block. This patient requires a pacemaker.
Triggered activity
there is an abnormality in the sequence of the action potential. Some areas are recovered and depolarize, while others are still repolarizing. 2 types: Early after depolarizations (EAD) and delayed after depolarizations (DAD).
Wolff Parkinson White syndrome
there is an accessory pathway that allows electrical activity to be conducted from atria to ventricle
Ventricular fibrillation
there is chaotic electrical activity in the ventricles, and there are no organized ventricular contractions (so the patient is pulseless). This leads to death. This can be the terminal rhythm for all the tachycardic arrhythmias (both SVT and VT), and it can be the primary rhythm with acute MI. Can be coarse or fine. People who are predisposed to get VF are given implanted defibrillators which detect VF and defibrillate within 5 seconds.
Changes that occur from lying→standing position
there is gravitational fall of circulating blood, & decreased stretch is felt in the carotid receptors. These receptors send an afferent signal to the brain and an efferent signals to limbs. Sympathetic stimulation increases and parasympathetic stimulation decreases, resulting in INCREASED HR and INCREASED VASOCONSTRICTION.
Hypertrophic cardiomyopathy
there is marked LVH without dilation, which leads to resistance to diastolic filling because the hypercontracted heart with slit-like ventricle (banana-like ventricle). All cases are genetic: 50% of cases are familial (autosomal dominant), and 50% of cases are due to sporadic mutations. There is asymmetric thickening, often in the subaortic region of the SEPTUM. Clinical picture: angina, atrial fibrillation w/ possible thromboembolism, mitral infective endocarditis, ventricular arrhythmias, or sudden death. Gross appearance: most of the thickening is in the septum, but the free wall is also thick. Histology: myocyte hypertrophy, interstitial fibrosis, and DISARRAY OF MYOCYTES (not in parallel bundles).
Low fat diet
there is no evidence to suggest that a low fat diet (<45 mg/day) reduces risk of developing CVD. People who follow low fat diet often replace calories from fat with calories from refined carbohydrates, which overall leads to increased incidence of DM and obesity. However, TYPE OF FAT in diet affects CVD risk.
Restrictive cardiomyopathy
there is reduced ventricular compliance due to stiffening of wall and failure of relaxation. This leads to increased resistance to diastolic filling. Systolic function is unaffected (so there is no hypertrophy). However, the atria dilate (due to increased resistance to diastolic filling of the ventricle). Can be caused by radiation injury/fibrosis, amyloidosis, sarcoidosis, idiopathic, inborn errors of metabolism, metastatic tumors. Gross image shows normal sized ventricle but very dilated atrium. Histology: shows myocytes with interstitial stuff (can be amyloid, sarcoid, or other things).
Low-calorie vegetarian vs Mediterranean diets for reducing body weight and improving cardiovascular risk
there is significant reduction in body weight, BMI, and fat mass for both vegetarian and Mediterranean diets. With Mediterranean diet, there was significant decrease in triglyceride levels. With vegetarian diet, there was significant decrease in LDL. Note: Mediterranean and vegetarian diets are both high in mono unsaturated fats. This reinforces the idea that the quality of fat is more important than the quantity of fat.
T-type calcium channels (I-Ca-T)
transient opening calcium channels that contribute to diastolic depolarization (pacemaker potential)
Treatment for aortic regurgitation
treat only if SEVERE. For aortic regurgitation: vasodilators (ACE inhibitors, CCBs, Nifedipine) can delay surgery, but surgery should be done.
Treatment for mitral regurgitation
treat only if SEVERE. For mitral regurgitation: refer for surgery.
Ventricular fibrillation: treatment
treatment is DEFIBRILLATION AND CPR (ALS protocol), and identify/treat the underlying cause (electrolyte abnormality, myocardial infarct, or degeneration of a primary arrhythmia)
Rheumatic heart disease
used to be very common, but in the US we use antibiotics for strep throat so it is less common now in industrial countries. Patients who get rheumatic heart disease are usually from less developed countries. Pathophysiology: Group A strep pharyngitis occurs, and the immune system makes antibodies against strep's M antigen that cross-react with proteins on valves, resulting in valvular stenosis or occasionally valvular insufficiency.
Subacute bacterial endocarditis
usually caused by VIRIDANS group streptococci (mouth flora), and they are caused by POOR DENTITION. The organism is not as pathogenic, so the presentation is much more INDOLENT (anemia, fatigue, worsening/new murmur, stigmata). It was heavily associated with heart damage from rheumatic fever. It is the minority of cases.
Right sided heart failure
usually caused by left sided failure, because backup from the left heart into the lungs (causing pulmonary HTN), which next overloads the right heart and causes cor pulmonale (right sided heart failure due to pulmonary hypertension). The right heart can't keep up with systemic venous return from the body, and there is SYSTEMIC & PORTAL VENOUS CONGESTION & EDEMA. This manifests as CHRONIC PASSIVE CONGESTION OF THE LIVER (nutmeg liver), distended neck veins, deep vein thrombosis & stasis dermatitis (superficial veins), pedal & pretibial edema ± pitting, Anasarca (total body edema), pericardial effusions, pleural effusions, ascites
Hydralazine
vasodilator that also prevents tachyphylaxis of nitrates. It does not lose their effects over time. Use of hydralazine perpetuates the effects of Nitrates.
Nonsustained ventricular tachycardia (NSVT)
ventricular tachycardia self-terminates within 30 seconds, and there is no hemodynamic collapse
Sustained ventricular tachycardia (NSVT)
ventricular tachycardia that lasts longer than 30 seconds or causes hemodynamic collapse (passing out from low BP)
Orthostatic hypotension
when Systolic BP decreases by >20 mmHg, diastolic BP decreases by >10 mmHg, or HR increases by >20 BPM by any positional change (lying→sitting, sitting→standing, or lying→standing).
STEMI
when the ST segment is elevated >1 mm in at least 2 contiguous leads (leads that are anatomically near each other-septal, anterior, inferior, lateral, posterior)
Aortic regurgitation/insufficiency: clinical case
younger patient, IV DRUG USER (tend to get infectious endocarditis), FEVER, CHEST PAIN, DYSPNEA. WIDE PULSE PRESSURE (SP>>DP). BOBBING HEAD (from rapid forward and backward flow in the aorta). PMI IS LATERALLY DISPLACED (due to LV dilation). S3 GALLOP AT APEX (due to volume overload of LV). High pitched, DECRESCENDO, BLOWING DIASTOLIC MURMUR at the LSB: subtle diastolic murmur at the left sternal border (because blood is regurgitating from the aorta back into the left atrium). EKG: you may see LVH. CXR: you may see LV enlargement with dilation downward and leftward.
Resting membrane potential for contractile cells
~-85 mV, which is due primarily to the opening of inward-rectifying potassium channels and high efflux of potassium ions. Does not reach the potassium equilibrium potential (-95 mV) because of background sodium "leak" current.
