week 2

reverse typical flutter

--Reverse typical flutter usually shows rounded or bimodal positive deflections in inferior leads II, III and aVF, and a very characteristic bimodal negative wave in the shape of a W is seen in lead V1. --Either spontaneously or after programmed stimulation, re-entry may occur in the opposite (clockwise) direction - i.e. superoinferior in the septal wall and inferosuperior in the anterolateral wall - with the same zones of block in the posterior RA and obligatory passage through the CTI (see Figure 3).19 This reverse typical flutter is much less common clinically than the counter clockwise form, but the clinical manifestations are indistinguishable. **normally, re-entrant goes counterclockwise, but it can reverse, but this is much less common

loss of y-descent

--V wave= passive filling of RA during RV systole --Y descent= TV opens, passive RA emptying --A wave= RA contraction --X descent= RA relaxation --with tamponade, blunted Y descent (lose the y and then you die) --passive emptying of RA is dependent on pressure difference between RA and RV--in tamponade there is equalization of diastolic pressures **passive filling of leaft ventricle from right atrium --here, filling into ventricle is NOT promoted bc diastolic pressures are equalized so you lose y descent

what conditions does digoxin treat?

--Ventricular Rate Control in Atrial Fibrillation --chronic heart failure --Paroxysmal Supraventricular Tachycardia

unstable angina

--a patient with chronic stable angina may experience a sudden increase in tempo and duration of ischemic episodes, occuring with lesser degrees of exertion and even at rest --can be a precursor of acute MI

what drugs are given as treatment for pericarditis?

--aspirin --ibuprofen --colchicine

clinical features of pericardial effusion

--asymptomatic --dull constant ache in left side of chest --findings of cardiac tamponade --compression of nearby structures leading to dysphagia, dyspnea, hoarseness, hiccups --heart sounds may be muffled --dullness to percussion of the left lung over the angle of the scapula may be present

silent ischemia

--asymptomatic episodes of myocardial ischemia --can be detected by electrocardiogram and other laboratory techniques

what is the etiology of atrial tachycardia?

--automatic/triggered, reentrant <<technically, atrial flutter and atrial fibrillation belong to this group, but clinically we exclude them and think of them separately can be: a. unifocal or multifocal b. sustained or paroxysomal **p wave is generated in atria in a site below the SA node --p wave may look like sinus p wave if generating site near SA node, but often morphology is slightly differnet --PR interval either normal or decreased depending on distance from generation site to AV node --Pwave rate usually 150-200 BPM --p waves may or may not be upright in I, II, aVF

what happens the the pressures in the heart with cardiac tamponade?

--because the heart is being compressed, the diastolic pressure within each chamber becomes elevated and equal to the pericardial pressure so they cannot accomidate the normal venous return so the systemic and pulmonic pressures rise --this leads to right-sided heart failure and pulmonary congestion --reduced filling of ventricles during diastole decreases the systolic stroke volume, and cardiac output declines --this leads to sympathetics being activated, but not able to help leading to shock and death

what cardiac conditions have palpitations as a symptom?

--bradycardia --tachycardia --ectopic beats

stable angina

--chronic stable angina manifests as a pattern of predictable, transient chest discomfort during exertion or emotional stress --generally caused by fixed, obstructive atheromatous plaque in one or more coronary arteries --pattern of symptoms is usually related to degree of stenosis --contributing to inadequate oxygen supply in stable angina is inappropriate coronary vasoconstriction caused by atherosclerosis-associated endothelial dysfunction --extent of coronary artery narrowing in patients with atherosclerosis is not always constant--it can vary from moment to moment bc of changes in superimposed coronary vascular tone

what are the normal pressure changes within the heart during breathing?>

--decrease in intrathoracic pressure is transmitted to pericardium and right atrium --IVC pressure now higher than RA which promotes right sided filling and shifts ventricular septum to the left --this slightly decreases LV filling/SV which leads to a small decrease in SBP --decrease in SBP by <12 mmHG is normal with inspiration

tamponade pressure changes

--during cardiac tamponade, changes in intrathoracic pressure are transmitted to pulmonary veins but not to pericardial sac --effective filling gradient falls during inspiration **doesn't get the change in pressure bc so full of fluid **filling gradient to fill the left side of the heart is decreased **leads to a drop in BP on left side

consequences of ischemia

--during ischemia, myocytes convert from aerobic to anaerobic metabolic pathways --reduced generation of ATP impairs the interaction of the contractile proteins and results in transient reduction of both ventricular systolic contraction and diastolic reaction, as each are energy-dependent processes --therefore, elevation of LV diastolic pressure is transmitted to pulmonary capillaries and can lead to pulmonary congestion and dyspnea --ischemic cardiac injury results in either irreversible myocardial necrosis or rapid and full recovery of myocyte function --can sometimes result in a period of prolonged contractile dysfunction without myocyte necrosis and recovery of normal function may ultimately follow

what symptoms are present in someone who is experiencing bradycardia?

--dyspnea --effort intolerance --fatigue --near syncope/syncope --chest pain/pressure

when should you hospitalize a patient with pericarditis?

--fever of greater than 38C --subacute onset --large pericardial effusion --cardiac tamponade --lack of response to treatment in 1 week --myopericarditis (+troponin) -> the myocardium and pericardium are affected --immunosuppression --trauma --oral anticoagulant therapy

what is the function of the pericardium?

--fixes heart within mediastinum --limits movement --prevents extreme dilation of heart when there is a sudden rise of intracardiac volume --absence of pericardium is often asymptomatic --can remove pericardium in patients that have a diseased pericardium and they seem to do ok, so not sure what the real function is

what are typical physical exam findings for someone with pericarditis?

--friction rub --sounds like walking on crunchy snow --heard best leaning forward in exhalation --use diaphragm of stethoscope ***comes and goes with one exam to the next classically, has 3 components: 1. ventricular contraction 2. ventricular relaxation 3. atrial contraction **need to listen frequently to diagnose bc it comes and goes

when do you administer adenosine?

--given to literally stop the patient's heart ***there is complete AV disruption for 90 seconds to completely isolate atrial conduction to see if flutter waves are present since there will be no QRS complexes since the AV node is blocked --therefore, this is used to diagnose atrial flutter and determine the degree of the block

prostacyclin

--has vasodilator properties similar to NO, but uses a cAMP dependent mechanism

when does a patient need treatment for bradycardia?

--if there is sinus node dysfunction where the ventricular rate is <40BPM --AV blocks with 2nd degree type II and 3rd degree as well as afib with greater than 5 second pause

pulsus paradoxus

--important physical sign of cardiac tamponade --can be recognized by standard BP cuff --decrease of systolic BP by more than 10 mmHg during normal inspiration --an exaggeration of appropriate cardiac physiology **drop in SBP >12 mmHG within inspiration --BP drop is enhanced --here, normal physiological response is exaggerated because increased LV interdependence because of pericardial restraint --ventricle cannot expand outside of restraint

under normal conditions, howe do coronary arteries respond to physical activity or mental stress?

--in normal persons, physical activity or mental stress results in measurable coronary artery vasodilation --NORMALLY, effect is regulated by activation of sympathetic NS with increased blood flow and shear stress stimulating the release of endothelin-derived vasodilators --the relaxation effect of NO outweighs the direct alpha-adrenergic constrictor effect of catecholamines on arterial smooth muscle, such that vasodilation results --in patients with dysfunctional endothelium, an impaired release of endothelial vasodilators leaves the direct catecholamine effect unopposed such that relative vasoconstriction occurs instead and therefore there is a decrease in blood flow leading to ischemia

what do the labs show of someone with pericarditis?

--increased WBC if viral or idiopathic --increased hs-CRP/ESR --increased troponin (usually indicated concomitant myocarditis)

what causes acute pericarditis?

--inflammation of the pericardium --viral infection --hypothyroidism/hyperthyroidism --neoplastic disease --radiation-induced --connective tissue disorders --drug induced --uremia (high BUN) --post-myocardial infarction --ect.

clinical features of cardiac tamponade

--jugular venous distension --hypotension with pulsus paradoxus = exaggeration of normal decline in systolic BP that occurs with inspiration --quiet precordium on palpation --sinus tachycardia

what are the causes of left axis deviation?

--left anterior fasicular block --INFERIOR MI --LEFT BUNDLE BRANCH BLOCK --paced beat --LEFT VENTRICULAR HYPERTROPHY --primum atrial septal defect --WPW --chronic lung disease

what are some signs and symptoms of atrial tachycardia?

--often associated with structural heart disease --may be asymptomatic --palpitations --chest pain --dyspnea

in what patients is bardycardia asymptomatic

--patient at rest --young patients have slower HR's --well conditioned individuals --patients will present with near syncope --heart rate is less than 60 BPM

unstable angina

--pattern of increased frequency and duration of angina episodes produced by less exertion or at rest --high frequency of progression to myocardial infarction if untreated

cardiac tamponade

--pericardial fluid accumulates under high pressure, compresses cardiac chambers and severely limits filling of the heart THEREFORE, ventricular stroke volume and cardiac output decline, potentially leading to hypotensive shock and death --any acute pericarditis can progress to cardiac tamponade, but most common causes are neoplastic, postviral, uremic pericarditis --acute hemorrhage into pericardium is also an important cause of tamponade which can result from: 1. blunt or penetrating chest trauma 2. rupture of left ventricle free wall following MI 3. as a complication of a dissecting aortic aneurysm

pressure volume graph for pericardial effusion

--pericardium is stiff --small increase in volume leads to a large increase in pressure on the heart

how to measure pulsus paradoxus at the bedside

--place BP cuff and inflate 20 mmHG above where radial pulse is no longer palpable --deflate cuff slowly --record pressure when the first Korotkoff sound is heard INTERMITTENTLY throughout respiratory cycle --continue to slowly deflate cuff --record the pressure when the Korotkoff sound is heard throughout the respiratory cycle **the difference between the two pressures is the pulsus paradoxus **when you hear the Korotkoff sound throughout the respiratory cycle, then you have found lower pressure **want to listen to heart sounds coming in and out with respiration --record all heart sounds heard

adenosine

--potent vasodilator and is though to be the prime metabolic mediator of vascular tone --decreases Ca2+ entry into cells which leads to relaxation, vasodilation, and increase in coronary blood flow

what are words used to describe palpitations?

--racing --fluttering --pause or skipping --quivering --thud or forceful beat --chest pain (RARE)

how does a patient present who has pericardial effusion?

--range of presentations from asymptomatic to shock (tamponade) --dysphagia --dyspnea --hoarseness --hiccups ***pulsus paradoxus **loss of y-descent on RA pressure tracing on exam: --muffled heart sounds --friction rub --ewart sign

electrical alternans

--refers to differential voltage from beat-to-beat or every few beats --most often appreciated in the QRS complex, but can be seen in P and T waves --causes: pericardial effusion and hypertrophic cardiomyopathy treat with a pericardiocentsis

myocardial infarction

--region of myocardial necrosis usually caused by prolonged cessation of blood supply --most often results from acute thrombus at site of coronary atherosclerotic stenosis --may be a first clinical manifestation of ischemic heart disease, or there may be a history of angina pectoris --irreversible damage to myocytes caused by prolonged ischemia and hypoxia as well as by reperfusion-induced injury --cause= occlusive thrombus usually resulting from plaque rupture in an epicardial coronary artery --damaged tissue is initially composed of a necrotic core surrounded by a marginal zone that can recover or become irreversibly damaged

nitric oxide

--regulates vascular tone by diffusing into and then relaxing neighboring arterial smooth muscle by cGMP-dependent mechanism

what are the causes of extreme (NW) axis deviation?

--right ventricular hypertrophy --VT --hyperkalemia --apical MI

paroxysmal atrial tachycardia

--some focus in the atria has taken over from the sinus node and causes the beats to be super irregular and there is long gaps --these "p waves" come out of nowhere --there are different p wave morphologies --then the heart goes back to normal and it can happen in cycles over and over

what is atrial fibrillation?

--supraventricular tachyarrhythmia with chaotic, uncoordinated atrial activity **no discernable p waves **fibrillation rate in atrium = 400-600 BPM **irregularly irregular rhythm --ventricular rate depends on 1. electrophysiological properties of the AV node 2. level of vagal and sympathetic tone 3. action of drugs --can present with rapid ventricular response (HR> 100) or controlled ventricular response (HR<100)

how does cocaine or other drugs, induce tachyarrhythmia?

--they increase the circulating NE levels by reuptake inhibition so there is more NE that can bind to beta 1 and beta 2 receptors and excite the cardiomyocyte **increases the workload and intraventricular pressure so this increases the chance that part of your heart will have low blood flow --every time it contracts, there is a higher pressure in ventricle and atria --more pressure is being pushed outward, so there is a great reduction in blood flow(lead to ischemia) --ischemia then sends out depolarizing signals to areas around the heart

hibernating myocardium

--tissue that manifests chronic ventricular contractile dysfunction due to a persistently reduced blood supply, usually bc of multi-vessel CAD --irreversible damage has NOT occurred and ventricular function can promptly improve if appropriate blood flow is restored by percutaneous or surgical revascularization

stunned myocardium

--tissue that, after suffering an episode of severe, acute, transient ischemia, demonstrates prolonged systolic dysfunction even after the return of normal myocardial blood flow --functional, biochemical, structural abnormalities following ischemia are reversible and contractile function gradually recovers

variant angina

--typical anginal discomfort, usually at rest, which develops bc of coronary artery spasm rather than an increase of myocardial oxygen demand --episodes often associated with transient shifts of ST segment, usually ST elevation

under normal conditions, who has a larger role in the constriction/dilation of arteries sympathetic or parasympathetic?

--under normal conditions, contribution of parasympathetic NS appears minor, but sympathetic receptors play an important role --coronary vessels contain both alpha and beta receptors *****stimulation of alpha receptors leads to vasconstriction *******stimulation of beta receptors leads to vasodilation

what is the mechanism of action for pharmacological therapy for acute treatment of bradycardia?

--use ANTICHOLINERGIC AGENTS--competitively bind to muscarinic receptors causing decreased vagal effect ie. atropine --beta receptor agonists--mimic effects of endogenous catecholamines ie. epi, dopamine, isoproterenol, dobutamine **interventions that change phase 4 ion conductances can change its slope **reduced funny current in SA nodal cells REDUCES heart rate

how to determine if the patient has cardiac tamponade

--use an echocardiography= most useful noninvasive technique to evaluate whether pericardial effusion has lead to cardiac tamponade **will see compression of right ventricle and atrium during diastole with high-pressure pericardial fluid **definitive diagnosis procedure for cardiac tamponade is cardiac catherization with management of intracardiac and intrapericardial pressures, usually combined with therapeutic pericardiocentesis --ECG --CXR --echocardiogram --heart catheterization--measure pressures

endothelin-1

--vasoCONSTRICTOR --production is stimulated by thrombin, angiotensin II, epinephrine, and shear stress of blood flow

EDHF

--vasodilator that effects neighboring smooth muscle cells

how do vasodilators interact with platelets?

--vasodilators released by endothelial cells also exert antithrombic properties by interfering with platelet aggregation therefore, in patients with damaged endothelium, they have procoagulation factors

What is the difference between STEMI and NSTEMI?

A STEMI or ST-elevation myocardial infarction is caused by a sudden complete (100 percent) blockage of a heart artery (coronary artery). A non-STEMI is usually caused by a severely narrowed artery but the artery is usually not completely blocked. The diagnosis is initially made by an electrocardiogram (ECG or EKG). In most situations, a patient having a STEMI needs to be treated immediately and this usually involves an emergent cardiac catheterization. A patient with a non-STEMI also often should undergo a cardiac catheterization but it may not have to be done immediately. Both types of heart attacks are serious and need prompt medical treatment.

what is the difference between type I and type II atrial flutter?

******Caused by a reentrant circuit in the atrium --flutter is normally at 300BPM --Type I (typical) - counterclockwise/clockwise circuit in RA around tricuspid annulus Type II (atypical) - other circuits in RA in the LA. Flutter rate = 250-350 bpm Most often 300 bpm Saw-tooth pattern in II, III, aVF (typical) ****normally, the patient gets AV block here since the AV node CANNOT conduct at rates of 300 BPM

what does the ECG look like for someone with pericarditis?

**diffuse ST elevation (except in aVR and V1) --this is a concave up or happy ST elevation --PR depression in leads with ST elevation

what is pericardial effusion, and what causes it?

**excess fluid in the pericardial sac --normal pericardial space has fluid, plasma or ultrafiltrate secreted by mesothelial cells that line serous layer --larger volume of fluid may accumulate with acute pericarditis causes: --same as pericarditis --post-open heart surgery --pulmonary hypertension --hemorrhagic trauma --decreased plasma oncotic pressure

what is rapid ventricular response?

In some cases of AFib, the fibrillation of the atria causes the ventricles, or lower chambers of the heart, to beat too fast. This is called a rapid ventricular rate or response (RVR). If you have AFib with RVR you'll experience symptoms, typically a rapid or fluttering heartbeat.

what are some conditions and medications that can cause bradycardia?

Medications: --Beta blockers (even beta blocker eye drops) ---Non-dihydropyridene --calcium channel blockers --Digoxin Conditions: --Hypothyroidism --Myocardial infarction --Pain/vagal response

what heart conditions uses a dual chamber pacemaker as treatment?

Used in patients with av block or if they need help in atria and ventricles

stable angina

chronic pattern of transient angina pectoris, precipitated by physical activity or emotional upset, relieved by rest within a few minutes --episodes often associated with temporary depression of ST segment but permanent myocardial damage does not result

ischemic heart disease

condition in which imbalance between myocardial oxygen supply and demand results in myocardial hypoxia and accumulation of waste metabolites, most often caused by atherosclerotic disease of the coronary arteries

how to treat cardiac tamponade

do a pericardiocentesis to remove fluid around the heart --prompt pericardiocentesis --send fluid for analysis of : cell count/differential, gram stain, cytology, triglycerides, adenosine deaminase for recurrent effusion, need surgery and pericardiectomy

what is the best treatment option for tachyarrhythmias?

electrical cardioversion (Shock) **only used if tachycardia is unstable = low BP, chest pain, syncope **do not use with sinus tachycardia --If you have a pulse, you give a synchronized rhythm -so when you press the shock button, it will administer the shock during the QRS complex to decrease bad --shocks are best for re-entrant arrhythmias --shock cancels out the re-entry to reset the heart --if you shock during t-wave to repolarize, you can go into ventricular arrhythmia

dysphagia

esophageal compression

what is the criteria for diagnosing pericarditis?

have to have two of the following: --chest pain --pericardial friction rub --ECG changes (ST elevation OR PR depression) --pericardial effusion

what heart conditions use a leadless pacemaker?

--For people that ONLY need pacing in the ventricles --Works for 8-10 years --Keep it in the heart forever --In inferior vena cava into the right ventricle and the it attaches to the right atrium bc it fuses with the endocardium --No wires in venous system --Leadless pacemaker

what needs to be on the ECG to diagnose multifocal atrial tachycardia (MAT)?

--HR needs to be greater than 100 --need at least 3 different p wave morphologies --results in an irregularly irregular rhythm --associated with underlying lung disease

what are some symptoms of tachycardia?

--Heart racing/fluttering --Heart vibration/quivering --Dyspnea --Lightheadedness --Syncope --Chest pain/pressure --Theses are all the symptoms of an anxiety attack, so if the pathology is normal, and these symptoms are all here with anxiety, then it could be a panic attack

what is normally the cause of atrial tachycardia with block?

--Often associated with digoxin toxicity where the atrial rate is accelerated and there is AV block

what are the causes of right axis deviation?

--RIGHT VENTRICULAR HYPERTROPHY --vertical heart --COPD --PULMONARY EMBOLISM --left posterior fasicular block --LATERAL MI --dextrocardia --limb lead reversal --secundum atrial septal defect --hyperkalemia --normal in infants and children

what non-cardiac conditions have palpitations as a symptom?

--Anxiety, Fear, Pain, --Depression --Fever --Hyperthyroidism --Anemia --Medications/drugs - stimulants --Pregnancy --Increased cardiac awareness

what tests should you run for pericardial effusion?

--CXR look for water bottle heart --echocardiogram --ekg look for alternans

what are clinical signs of atrial fibrillation?

--Can be asymptomatic --Palpitations --Chest pain --Fatigue --Dyspnea --Congestive heart failure (CHF) --: embolic stroke, systemic emboli From left atrial thrombus (usually in left atrial appendage)

what are the treatment differences for a patient with acute myocardial infarction and myocardial infarction with non-obstructive coronary arteries?

1. acute myocardial infarction is associated with obstructive coronary artery disease in over 90% of patients --these patients have good treatments established 2. patients with myocardial infarction with non-obstructive coronary arteries do not have good treatment options since coronary revascularization is not appropriate and the etiology of the infarct is not immediately apparent

2 ways the abnormal endothelial cell function can contribute to the pathophysiology of ischemia

1. by inappropriate vasoconstriction of coronary arteries 2. through loss of normal antithrombic properties

2 common causes of decreased myocardial oxygen supply

1. decreased perfusion pressure due to hypotension 2. severely decreased oxygen content --profound increase in myocardial oxygen demand can cause ischemia even in the absence of coronary atherosclerosis

how does a patient present with pericarditis?

1. fever 2. pleuritic, sharp chest pain that gets worse laying down and with a deep breath or a cough --radiates to the back, left trapezius muscle --better leaning forward, worse laying back

noninflammatory serous effusions may result from:

1. increased capillary permeability 2. increased capillary hydrostatic pressure 3. decreased plasma oncotic pressure

what are the three different types of irregularly irregular tachycardia?

1. multifocal atrial tachycardia 2. atrial fibrillation 3. atrial flutter with variable block

clinical features of a large pericardial effusion

1. soft heart sounds 2. reduced intensity of friction rub 3. ewart sign (dullness over posterior left lung)

3 factors that determine whether the pericardial effusion remains clinically silent or whether symptoms of cardiac compression ensure:

1. volume of fluid 2. rate at which fluid accumulates 3. compliance characteristics of pericardium **in chronic elevation of volume slowly overtime, the pericardium can adapt to hold more fluid and be ok

pharmacological therapy for tachyarrhythmias

Antiarrhythmic medications: a.Class I - sodium channel blockers b. Class II - beta blockers c. Class III - potassium channel blockers d. Class IV - calcium channel blockers Adenosine For tachyarrhythmias that traverse the AV node(hyperpolarizes cells in AV node to get complete AV block for a short period of time) Others: Digoxin, Magnesium(drug of choice for TdP)

what are the different types of tachyarrhythmias?

Atrial tachycardia Atrial Fibrillation Atrial Flutter Ventricular Tachycardia Ventricular Fibrillation Supraventricular Tachycardia WPW Syndrome

what channel in SA nodal cells does intracellular cAMP affect to change the phase 4 slope and heart rate?

HCN channel

when to use indirect MFR vs direct MFR

INDIRECT: --acute injuries --severe pain --patient apprehension --autonomic normalization --works on muscle spindles DIRECT: --chronic tension --rehabilitation from injuries --stretch trial before home exercise RX --patient preference

does unifocal atrial tachycardia have an irregularly irregular rhythm?

NO regular rhythm

in what portions of the ECG is the baseline voltage shifted from an ischemic sit's injury current?

PR interval TP segment

A small portion of the myocardium develops an inward calcium current that is active during phase 4 of myocyte action potential. during what portion of the ECG will this current have an effect?

PR segment because of the injury and the ischemia

acute coronary syndromes

acute coronary syndromes= unstable angina + acute MI --most commonly result from unstable atherosclerotic plaque with subsequent platelet aggregation and thrombosis

what does PR interval elevation indicate?

atrial infarction

what should be used to treat a patient with severe, symptomatic bradycardia?

atropine

in what direction is the net ion current from forward mode Na/Ca exchanger activity? does it cause depolarization or hyperpolarization of the cardiac myocyte?

inward flow and depolarization **the NCX channel is active at the peak of phase 0 so it has to depolarize --sodium enters down its concentration gradient and 1 sodium is the net rate of this exchange --high activity of NCX can lead to early afterdepolarizations and delayed afterdepolarizations

do smaller or larger vessels normally collect plaque?

larger vessels normally have plaque, and the smaller ones do not

dyspnea

lung compression

if a patient is symptomatic with bradycardia, what are they likely to report?

near syncope

what drugs cause drug-induced pericarditis?

need to know --procainamide --hydralazine --methyldopa --isoniazid --phenytonin --anthracycline chemotherapy agents --minoxidil --cyclosporine

what heart conditions uses a single chamber pacemaker as the treatment?

patients with a fib

what does PR interval depression indicate?

pericarditis

angina pectoris

uncomfortable sensation in the chest and neighboring anatomic structures produced by myocardial ischemia

how do you treat acute, symptomatic bradycardia?

with a pacemaker (device therapy)