Cardiac

Ventricular Function Curves

-A ventricular function curve is a plot of some index of ventricular function (stroke volume, stroke volume index) verses some measurement of end-diastolic volume (aka. PCWP, left ventricle preload) -when there is a increase or decrease in preload, there is a shift up or down of a single ventricular curve respectively --When there is an increase in contractility or a decrease in after load, there is an upward and to the left shift in the ventricular function curve (reflecting an increases in stroke volume and a decrease in the size of the left ventricular chamber) -Where there is a decrease in contractility of an increase in after load, there is a downward and to the right shift in the ventricular function curve (reflecting a decrease in stroke volume and an increase in the size of the left ventricular chamber) PCWP increases: SV: increase preload increases decrease contractility decreases increased after load decreases PCWP decreases: SV: decreased preload decrease increase contractility increase decreased after load increase

Cardiac Catherization for Ablation

-Major risks of cardiac catheterization include cardiac ischemia, vessel trauma, coronary dissection, thromboembolic events, and renal damage or allergic reaction related to the use of contrast dye. Diabetics are particularly susceptible to renal damage from the overuse of radio-opaque contrast dye -Of significant importance is the use of esophageal temperature monitoring during EP procedures. If the patient's temperature increases by as little as 0.1 degree Celsius, the electrophysiologist must temporarily but immediately cease the procedure and cool the tip of the catheter tip.

Congestive Heart Failure

-Patients with congestive heart failure often exhibit HYPONATREMIA due to activation of the vasopressin system (increases H2O reabsorption and dilutes Sodium, decreasing CONCETRATION: C= m/v --> increase V, decrease C; indirect). -Treatment with diuretics to reduce vascular fluid volume may also lead to hypokalemia and hypomagnesemia. -The triple therapy drug regimen used for patients with congestive heart failure consists of an ACE inhibitor, a beta-blocker, and a diuretic (which is often an aldosterone antagonist). -Compensatory mechanisms: Increased preload and sympathetic tone, activation of the renin- angiotensin system, and ventricular hypertrophy are the compensatory mechanisms that occur in the presence of heart failure. Because of the chronically increased levels of circulating catecholamines associated with congestive heart failure, the response of adrenergic receptors is diminished (down- regulated). As heart failure ensues, the ejection fraction decreases. As the left ventricle dilates, it accommodates more volume. Thus, the same ejection fraction of an increased volume will still be a normal stroke volume. As venous congestion and ventricular dilatation continues, however, clinical deterioration will eventually occur. -In congestive heart failure, sympathetic activation is increased, which results in increased secretion of norepinephrine. Circulating vasopressin levels are nearly twice the normal value in patients with congestive heart failure. Natriuretic peptide levels increase as the ventricles become the principal source the the hormone's release. The chronic increase in circulating catecholamines produces widespread arteriolar vasoconstriction which shunts blood away from the skin, gastrointestinal tract, heart, and brain. As blood flow to the kidneys decreases, the renin-angiotensin- aldosterone axis is activated which results in sodium retention and interstitial edema.

Pulmonic Stenosis

-Pulmonic stenosis produces obstruction to right ventricular outflow. -The objective in managing pulmonic stenosis is to: --prevent increases in right ventricular oxygen requirements. --prevent increases in heart rate and myocardial contractility. Because increases in pulmonary vascular resistance have little effect on the fixed obstruction of the pulmonic valve, the increase in PVR seen with positive pressure ventilation has little effect on patients with pulmonary stenosis.

Essential HTN vs. Secondary HTN

-Secondary hypertension is an increase in blood pressure due to a cause that can be identified and cured such as pheochromocytoma, renal artery stenosis, coarctation of the aorta, Conn's syndrome, or Cushing disease. --> Renal artery stenosis is the most common cause of secondary hypertension. -Essential hypertension is an increased blood pressure for which there is no identifiable cause and is diagnosed based on the exclusion of causes such as those listed above. Approximately 95% of patients with hypertension are diagnosed with essential hypertension.

Chronic Aortic Stenosis

-With chronic aortic stenosis, CONCENTRIC hypertrophy permits the left ventricle to generate greater pressure, but LV volumes remain about the same as normal, the PV loop shifts upwards -The exposure of the left ventricle to the increased pressure gradients associated with aortic stenosis result in concentric hypertrophy of the left ventricle (thickening of the ventricle wall). Management: HR: lower rhythm: NSR (no a fib) preload: maintain after load: maintain (preserve coronary perfusion) contractility: maintain AV area = 2-4 cm^2 severe < 0.8 -1.0 critical < 0.5-0.8 -narrowing, stenosed valve resulting in fixed left ventricle outflow tract obstruction -Concentric hypertrophy and increased LV pressure overload -decreased aortic root pressure -decreased coronary perfusion (increased O2 demand -LV ischemia -LV failure -decreased LV output -pulmonary edema etiology: -degenerative form: calcific aortic stenosis -bicsupid aortic valve s/s: ASD -angina -syncope -dyspnea on extertion Treatment: -relies on atrial kick -avoid increase in HR -reduced ventricle compliance may create a fixed SV--> CO relies on HR -hypotension treated with phenylephrine - SYSTOLIC MURMOR heard at right second intercostal space with transmission into the neck over the aortic arch -r wave progression on ECG --> LV hypertrophy *In aortic stenosis, left ventricular compliance decreases (less filling, less time meeting bodys demands, less ejected) as the left ventricle hypertrophies, resulting in diastolic dysfunction. -diastolitc heart failure can result in a preserved ejection fraction because both the blood ejected and the blood filled are decreased (same EF= dec SV/dec EDV *Aortic stenosis is the narrowing of the aortic valve which results in obstruction of blood flow into the aorta. It is the result of degeneration and calcification of the leaflets of the aortic valve or the presence of a bicuspid rather than a normal tricuspid valve. *The decreased pressure gradient that exists between the left atrium and left ventricle in aortic stenosis limits left ventricular filling dramatically. Because left ventricular filling is so dependent upon atrial contraction, loss of atrial systole can result in congestive heart failure or hypotension

WOLF PARKINSON WHITE SYNDROME

-defect in the cardiac conduction system -extra conduction pathway: BUNDLE OF KENT--> allows the transmission of electrical impulses via an abnormal circuit -abnormal pathway does not possess a rate-controlled characteristic like the SA and AV node -via this pathway rates can be extremely rapid, typically 150-250 bpm -premature electrical impulse usually triggers and episode of WPW -electrical circuit can travel either retrograde, or anterograde -anterograde: accessory pathway is refractory during the premature triggering impulse and the electrical current passes through the Purkinje fibers, reaches the accessory pathway and travels in a loop in the opposite direction -diagnoses by the presence of a delta wave on the ECG when the patient is asymptomatic (has a normal heart rate) -The QT interval is normally > 0.10s and the QRS appears slurred by the delta wave -volatile anesthetics increase anterograde refractoriness in both normal and accessory pathways and increase the ability of an extrasystole to trigger tachycardia -agents that increase sympathetic tone, such as ketamine, robinol, atropine, pancuronium, and sympathomimetics should be used with cation or avoided if possible -light anesthesia, hypercapnia and acidosis can trigger the sympathetic system and increase the likelihood that as extrasystole will result in tachycardia -deep anesthesia prior to intubation -AVOID VERAPAMIL (CC blocker) and DIGOXIN: which could enhance anterograde conduction through an accessory pathway -treatment of any arising dysrhythmia with beta blocker, adenosine and/or amiodarone (potassium channel blocker When preparing the patient with WPW for anesthesia, have the patient continue taking antidysrhythmics up to the day of surgery, avoid situations that could result in sympathetic outflow such as pain or hypovolemia, avoid verapamil or digoxin (which could enhance anterograde conduction through an accessory pathway) in the treatment of any arising dysrhythmia, and have adenosine, and/or amiodarone available for treatment of tachydysrhythmias

Nitric Oxide

-gastric substance produced by numerous tissues in the body -the enzyme nitric oxide synthase, converts the amino acid arginine to nitric oxide -3 forms of nitric oxide synthase -main interest is NO role as a vasodilator 1) a number of signals/chemicals stimulate nitric oxide synthesis (acetylcholine, bradykinin, calcium) 2) Nitric oxide synthase (NOS) converts L-arginine (amino acid arginine) to NO in the endothelial cell 3) the nitric oxide diffuses from the endothelial cell to the underlying vascular smooth muscle cell 4) in the smooth muscle cell, NO activates an enzyme: soluble guanylyl cyclase (sGC) 5) sGC converts guanosine triphosphate (GTP) to the second messenger cyclic guanosine monophosphate (cGMP) 6) cGMP causes smooth muscles to relax

Eccentric LV hypertrophy

-left ventricle wall stay the same -dilated left ventricle chamber -VOLUME OVERLOAD Causes: -chronic AR -chronic MR -morbid obesity (increase in plasma blood volume)

Nitric Oxide donation

-sodium nitroprusside, nitroglycerine, and dinitrates "DONATE" NO molecules at the vascular wall to promote VASODILATION -The NO released diffuses through the vascular endothelium to the vascular smooth muscle where it actives sGC which in turn converts GTP to cGMP -In essence, the donated NO "bypasses"the endothelial cell biochemistry (Nitric oxide synthase (NOS) converts L-arginine (amino acid arginine) to NO in the endothelial cell) and diffuses directly to the smooth muscle

Concentric Hypertrophy of Left Ventricle

-thicker left ventricle wall -normal LV chamber -PRESSURE overload Causes: -chronic untreated hypertension -chronic aortic stenosis (build up of pressure) -coarctation of the aorta

Baroreceptor Reflex

1) Increase in arterial blood pressure 2) Increase stretch of baroreceptors in carotid sinus an aortic arch 3) Increase action potential in afferents (toward brain) of vagus nerve (from aortic arch and Hering's Nerve (a branch of the glossopharyngeal) from carotid sinus to CARDIOVASCULAR centers in the medulla of brainstem 4a) Increase in action potentials in efferent (away from brain) vagus nerve --> decrease HR, decreased CO 4b) decreased sympathetic nerve acton: -decreased HR (decreased contractility, SV and CO) -venous blood vessels (ventilation, decreased preload (venous return), decrease CO -arterial blood vessels (decrease SVR) 5) Result: decreased in arterial blood pressure BAROREPCEPTORS have to do with response to pressure

Summary of difficult concepts

1. When preload increases or decreases, EDV increases (PCWP increases) or decreases (PCWP decreases), but the amount of blood in the chamber at end systole dose not change; thus SV increases or decreases 2. When SV falls either as a result of increased SVR or decreased contractility, the heart empties less effectively and the blood in the chamber increases (PCWP increases) and the chamber dilates --> "if you don't pump if forward, you leave it behind" 3. When SV increases either as a result of decreased SVR or increased contractility, the heart empties effectively and the blood in the chamber decreases (PCWP decrease) and the chamber "shrinks"

Edema Formation

1. increased plasma hydrostatic pressure: a. Right heart failure promotes systemic edema b. left heart failure promotes pulmonary edema 2. Decreased plasma colloid osmotic pressure, hypoalbuminemia cause by liver disease increases edema 3. lympathic obstruction

Conduction pathway through the heart

1. sinus node: normal pacemaker 2. Internodal tracts a. anterior internodal (Bachmann's bundle_ b. middle internodal tract c. posterior internodal tract 3. AV node (delays action potential) 4. Atrioventricular (common) bundle of HIS 5. Bundle branches a. left bundle i. anterior fascicle ii. posterior fascicle b. right bundle 6. Purkinje fibers 7. Ventricular muscle NOTE: -action potential in the sinoatrial node and in the atrioventricular node are BIPHASIC (they have depolarization and depolarization phases and no plateau phase -acton potentials with PLATEAU phases are found in atrial muscle cells and ventricular muscle cells

Aortic Regurgitation

Acute vs Chronic: PV loop: AV fails to close completely, isovolumetric relaxation is no longer isovolumetric (left side of the loop), some blood leaks back into the ventricle during systole -with aortic insufficiency (regurgitation), the volume in the left ventricle chamber increases during early diastole -The early relaxation phase of the pressure-volume loop is not isovolumetric -in acute aortic regurgitation, the pressure loop is small -With chronic aortic insufficiency, the left ventricle hypertrophies (eccentric) and the left ventricle chamber dilates and the pressure volume loop is large because the stroke volume is large Management: Heart rate: increased rhythm: NSR Preload: maintain Afterload: decrease Contractility: maintain Pathophysiology" -regurgitation of some ejected stroke volume from aorta back into the left ventricle during diastole which leads to left v fluid overload and pressure overload -either congenital or due to rheumatic fever -acute aortic regurgitation is more commonly seen following infective endocarditis, trauma, or aortic dissection -regurgitant volume depends on heart rate, the diastolic pressure gradient across the aortic valve, and the aortic valve orifice -over time chronic regurg results in Lv to retrain a large regurgitant volume and there will be no room for atrial volume -The hallmark characteristic of aortic regurgitation is ECCENTRIC left ventricle hypertrophy --> large ventricular compliance -Aortic regurgitation results when the aortic leaflet fails due to disease of the aortic root or of the leaflet itself. It results in a decrease in cardiac output because of regurgitation of a portion of the ejected stroke volume back into the left ventricle. The left ventricle compensates by becoming hypertrophied and enlarges to accommodate the fluid volume overload. s/s: (may be asymptomatic) -angina can occur in the absence of CAD d/t increased myocardial O2 demand -exertional dyspnea -orthopnea -paroxysmal nocturnal dyspnea -DIASTOLIC Murmor: left sternal border -bouding peripheral pulses -widened pulse pressure (decreased DBP) Acute: -sudden onset pulmonary edema -hypotension -SOB -weakness Chronic: -CHR -symptoms minimal with regurgitant volume < 50% SV, but severe if > 50% SV Treatment: -most patients tolerate spinal or epidural if intravascular volume is maintained -pancuronium prevents bradycardia -ephedrine is vasopressor of CHOICE -avoid myocardial depression, tachycardia, increased DBP, too much preload and too high of a heart rate -decrease SVR to promote forward flow *An increase in the diastolic blood pressure increases the backward pressure gradient which results in an increase in the proportion of stroke volume that regurgitates back into the left ventricle

Mitral Regurgitation

Acute vs. Chronic PV loop: - mitral valve fails to close efficiently during systole, isovolumetric contraction is no longer isovolumentric (right side of the loop), some of the blood in the left ventricle leaks back into the left atrium during contraction -the volume in the left ventricle decreases during early systole -the early systolic phase of the pressure-volume loop is not isovolumetric in mitral regurgitation -in acute mitral insufficiency the pressure volume loop is small -with chronic MVR the left ventricle hypertrophies (eccentric) accordingly and the left ventricle chamber dilates and the pressure volume loop is large because stroke volume is large Management: HR: increase Rhythm: NSR Preload: Maintain Afterload: Decrease Contractility: maintain -decreases in forward LV stroke volume -decreased CO -increased left Atrial pressures and volume -pulmonary vascular congestion Etiology: -rheumatic fever (chronic) -myocardial ischemia/infarction -infective endocardities -chest trauma -Left ventricle compensates by dilating (ECCENTRIC)and increased EDV--> EDV remains normal but eventually increases as the disease progresses -by increased EDV, the volume overloaded left ventricle can maintain a normal cardiac output even as the ejection fraction decreases Symptom progression (rule of 1/3s) -regurgitant factor < 30% = mild s/s -regurgitant factor 30-60% = moderated s/s -regurgitant factor > 60% = severe Blowing, holosystolic murmur best heard at apex, with radian to the axilla Treatment: -watch fluids (pulmonary edema) -avoid decreased HR, myocardial contractility -Afterload reduction -surgical repair suggested with EF is < 60% -spinal/edpidural may be ok -inotropes increases contractility, vasodilators decrease SVR Monitor: -V wave: prominent during acute deterioration, represents left atrial compliance in relationship to the regurgitant volume Mitral regard has a regurgitation volume that is based on mitral valve size, heart rate, and pressure gradient between atria and ventricle *Acute mitral regurgitation can occur as a result of myocardial infarction, papillary muscle dysfunction, chordae tendinae rupture, trauma to the chest, or infectious endocarditis.

Systemic Vascular Resistance/Afterload

Afterload is the tension (force) in the wall of the heart at the time the aortic valve opens -determined by systemic vascular resistance (PRESSURE) -the greater the SVR, the greater the after load Left sided after load -inverse relationship with SV -increase in SVR, decreased in SV, therefore decrease in CO

Mechanical Obstruction of the Trachea

All start with A -Aberrant left pulmonary artery, double aortic arch (aortic arch x 2), and absent pulmonic valve all create the potential for mechanical obstruction of the trachea.

Mitral Valve prolapse

Any factor that maintains a larger ventricular volume will decrease the degree of prolapse. Hypertension, vasoconstriction, drug-induced myocardial depression, and increased preload will decrease the degree of prolapse. -Mitral valve prolapse is associated with a midsystolic click and a late systolic murmur.

Murmor Master

Ass Arch Mr. SA Ms. DA ARDS Ass Arch = aortic stenosis, systole, aortic arch ARDS= Aortic regurgitation diastolic sternal border Ms. DA = Mitral stenosis, diastolic, apex Mr. SA = Mitral regurgitation, systolic, apex

Cardiac Tamponade

BECK's Triad: -hypotension -distant heart sounds -distendend neck veins -obstruction of right atrial filling, central venous pressures increase resulting in distended neck veins unless severe hypovolemia is also present. -Hypotension develops as cardiac output drops -tachycardia often ensues as a compensatory mechanism (sympathetic response) -Electrical alternans is a variation in the ECG caused by the shifting of the heart within the distended pericardium as it beats. -Kussmauls sign and pulsus paradoxus are both indicative of ventricular discordance (also known as ventricular dyssynchrony) that occurs due to the opposing response of the ventricles to filling during the respiratory cycle. -The primary goals in the management of a patient with symptomatic cardiac tamponade include: expanding intravascular volume by administering crystalloids or colloids, maintaining heart rate and contractility by administering catecholamines (including isoproterenol), administering dopamine to increase systemic vascular resistance if necessary, administering atropine to prevent vagal reactions to the increased intrapericardial pressure, and correcting metabolic acidosis (metabolic acidosis can have detrimental effects on cardiac contractility). *Constrictive pericarditis is similar to cardiac tamponade in many of its features. They both exhibit pulsus paradoxus and Kussmauls sign. Pulsus paradoxus is more common in patients with tamponade. *Induction is typically carried out with ketamine because it increases heart rate, contractility, and systemic vascular resistance. A benzodiazepine is often combined with it. The anesthetic may be maintained with nitrous oxide and fentanyl combined with pancuronium, which is useful for its vagolytic effects. *The combination of peripheral vasodilation and myocardial depression from the anesthetic and decreased venous return from positive pressure ventilation can produce severe, life-threatening hypotension in the patient with cardiac tamponade.

RATE of PHASE 4 Depolarization

Changing the slope of phase 4 depolarization causes heart rate to change: -when HR is slowed by acetylcholine (parasympathetic activation), it takes longer to reach threshold, so there is longer time between potentials, hence HR is decreased -when phase 4 depolarization is accelerated by norepinephrine (sympathetic activation), threshold is reached more quickly, so there is less time between action potentials, HR increases Changing the RATE of PHASE 4 DEPOLARIZATION leads to a change in HR

Myocardial contusion

Chest pain, palpitations, dysrhythmias, ST and T wave abnormalities, and elevated LDH, creatine kinase, and troponin levels are all consistent with myocardial contusion. _Myocardial contusion exhibits ST and T wave abnormalities.

Endocarditis

Chronic tonsillar infection places the patient with cardiac valvular disease at risk for endocarditis due to chronic streptococcal bacteremia. -amoxicillin PO is the antibiotic of choice ( ceftriaxone, cephazolin IM or IV may also be used) -prophylaxis to a patient at risk is not recommended for upper or lower gastrointestinal endoscopic procedures.

Terms

Chronotrophy: rate of depolarization Dromotrophy: rate of conduction Inotrophy: degree of contractility Lusitrophy: vary the degree of contractility

Cor Pulmonale

Cor pulmonale is a sequence of symptoms that originate with hypoxia due to pulmonary pathology, often COPD. The hypoxia results in hypoxic pulmonary vasoconstriction and elevated pulmonary artery pressures. In the face of pulmonary hypertension, the right ventricle can begin to fail resulting in PROMINENT A waves on the central venous pressure, jugular venous distention, hepatosplenomegaly, peripheral edema and often a diastolic murmur due to incompetence of the pulmonary valve. -Electrocardiographic signs consistent with cor pulmonale include peaked P waves in leads II, III, and aVF which are consistent with right atrial hypertrophy and right axis deviation and right bundle branch block which are consistent with right ventricular hypertrophy. *The chest xray often reveals increased width of the right pulmonary artery and decreased pulmonary vascular markings in the lung periphery. A late sign of cor pulmonale may be a decrease in the retrosternal space on the lateral film as right ventricular enlargement becomes evident. *Eisenmenger's syndrome is defined by the reversal of a left-to-right shunt when pulmonary vascular resistance increases above that of systemic vascular resistance. -Eisenmenger's syndrome is a reversal of a left-to-right intracardiac shunt due to an increase in the pulmonary vascular resistance. Once the pulmonary vascular resistance reaches a level that is equal to or exceeds systemic vascular resistance, the shunt reverses to a right-to-left shunt.

Cardiac Output

Determined by HR and SV CO= HR x SV or rearrange SVR calculation: CO= (MAP-CVP)/SVR (Flow= change in pressure over a resistance; Higher the resistance, lower the cardiac output, higher the change in pressure, higher the CO) Measuring cardiac output by Thermodilation: -Cardiac output is inversely proportional to the area under the therm-dilation curve -the smaller the area, the greater the CO -the larger there area, the smaller the CO

Mean Arterial Pressure

Determined by cardiac output and systemic vascular resistance MAP= SBP - 2DBP/3 Diasolte = 2/3 of CO

Stroke Volume

Determined by the interplay of three factors: -preload -afterload -contractility SV= EDV-ESV SV= Co/HR

Increased Contractility

Digitalis: slows phase 4 depolarization in SA and AV node thereby decrease automaticity @ the AV node; increases intracellular calcium concentration increasing contractility PDE inhibitor: decreases the breakdown of cAMP, thereby increasing Ca in the heart and increasing contractility Both drugs increase inotrophy!!!! -When contractility increases, the ventricle empties more completely --end systolic volume decreases more than end diastolic volume decreases (both decrease but one more than the other), so SV INCREASES -the ventricle chamber "shrinks", LV volume decreases -Blood pressure increases due to increased contractile pressure/force at which ejection occurs -a decrease in PCWP provides evidence that end diastolic volume has decrease -heart rate may decrease reflexively (also due to the parasympathetic effects of digoxin) -SVR may reflexively decrease -PV loop: ---shifts to the left due to decrease in LV volume (EDV & ESV) ---increases in height due to increase contractility and blood pressure ---widens due to increase in SV Summary: -contractility increases -end diastolic volume decrease -end systolic volume decreases the most -SV increases -LV volume shrinks -PCWP decreases -HR reflexively decreases -SVR reflexively decreases

Nonadrenergic Cardiovascular Drugs

Direct Acting Vasodilators: -Hydralazine (Apresoline): arterial dilator (decreased SVR) -Diazoxide (Hyperstate): arterial dilator (can cause hyperglycemic coma) -Nitroglycerin: venodilator (decreases preload) -Nitroprusside (Nipride): arterial and venous dilator (decrease preload and after load) Calcium Channel Blockers: -Verapamil (Calan, Isoptin): arterial dilator, slow phase 4, decreased HR -Diltiazem: arterial dilator, decreases HR -Nifedipine (Procardia): arterial dilator may cause reflex tachycardia ACE Inhibitors (prevent conversation of angiontensin I to angiotensin II [potent vasoconstrictor]): -Captopril (Capoten): arterial dilator -Enalaprin (Vasotec): arterial dilator Phosphodiesterase (PDE) Inhibitors (positie inotropes): -Inamrinone (Inocor) & milrinone (Primacor): block breakdown of cAMP, increase cardiac calcium and increasing myocardial contractility, cAMP decreased Ca at smooth muscle which causes decrease in SVR and relaxes vascular smooth muscle: vasodilation Adenosine: -endogenous nucleotide occuring in all cells of the body, can be administered to: -slow conduction of impulses through the AV node -interrupt reentry pathways throught the AV node -restore normal sinus rhythm in patients with paroxysmal supra ventricular tachycardia, including the associated WPW syndrome. -Adminstration of adenosine 6-12 mg as a RAPID injection usually converts SVT to NSR within one minute -this dose has no hemodynamic effects -elimination hald time is less than 10 seconds owing to rapid metabolism

Bainbridge Reflex Related to inspiration/expiration

During inspiration heart rate increases: -inspiration: the diaphragm moves down decreasing intrathoracic pressure and lowering right atrial pressure thus facilitating venous return -the right atrium stretches and reflexively the heat rate increases (Bainbridge reflex) During expiration heart rate deacreases -expiration: the diaphragm moves up, increasing intrathoracic pressure and increasing right atrial pressure thus decreasing venous return Similar mechanism: During the bainbridge reflex, the superior vena cava dilates and venous pressure falls, and venous return increase --> the key concept here is "pressure gradient" =, fluids and gases flow when there is a pressure gradient and flow is directly proportional to the pressure gradient. When venous pressure decreases, the pressure gradient across the system increases, thus venous return flow increases BAINBRIDGE has to do with return of blood to the heart

TOF

Factors that can increase the right-to-left shunt in a patient with tetralogy of Fallot include: 1. An increase in myocardial contractility 2. An increase in pulmonary vascular resistance 3. A decrease in systemic vascular resistance. -Atrial fibrillation, atrial flutter, right bundle branch blocks, and ventricular dysrhythmias are all common following surgical correction of tetralogy of Fallot. Third-degree block is very uncommon following this procedure.

AV Heart Block

First Degree: PR > 0.20 Second Degree Type 1: PR longer, longer drop (Wenckebach) -Wenckebach (also known as Mobitz Type I second degree block) is characterized by a heart rate between 60 and 100 beats per minute, a regular atrial rhythm, a variable ventricular rhythm, and a PR interval that progressively lengthens until a QRS complex is dropped completely. It is commonly seen in highly trained athletes and with drug toxicity. Second Degree Type II: PR are regular but some are not followed by QRS Third Degree: both PR and QRS are normal but they are independent from each other

Decreased Contractility

Heart Failure: unable to contract effectively and push blood forward -When contractility decrease, the ventricle empties less completely -End diastolic volume increases -end systolic volume increase due to lack of effective pump -the LV dilates -Stroke Volume decreases -Blood pressure decreases due to the decreased LV pressure at which ejection occurs -Heart rate may reflexively increase -SVR may reflexively increase -an increase in PCWP provides evidence that the LV end diastolic volume has increases -PV loop: --shifts to the right due to increases in both EDV & ESV --decreases in size due to lower force of contractility and decrease in blood pressure --narrows due to decrease in SV Summary: -decreased contractility -increased EDV -increased ESV -decreased SV -increase in PCWP -increased in HR -increased in SVR -increased LV volume

Potassium ECG disturbances

Hyperkalemia: peaked, or tented, T waves Hypokalemia: depressed T waves, U wave present

Hypertensive Emergency

Hypertensive emergency is defined as hypertension with evidence of end-organ damage such as: -myocardial ischemia -dissecting aortic aneurysm -renal insufficiency -pulmonary edema -encephalopathy -eclampsia -intracerebral hemorrhage. Hypertension without signs of end-organ damage is termed 'hypertensive urgency'. These patients often present with hypertension and symptoms such as: -headache -epistaxis -anxiety. **The exception to the rule is parturients. A parturient with a diastolic blood pressure greater than 109 mmHg is defined as being in a state of hypertensive emergency even if no other symptoms are present.

Increased preload

Intravenous Fluid Bolus (Increased Preload): -when end diastolic volume increases (preload increases), the left ventricle empties to the previous end systolic volume. -consequently, with greater filling but emptying back to the previous level, SV increases (thus CO and MAP increase) -PV loop is wider due to increased volume and taller due to increased pressure **An increase in pulmonary capillary wedge pressure provides evidence of the increase in end-diastolic volume aka increase in preload HR may reflexively decrease d/t the baroreceptor reflex SVR may reflexively decrease d/t the baroreceptor reflex Summary: -increase preload -increased EDV -increased PAWP -same ESV -increased SV -increased CO -increased MAP -reflux DECREASE in HR -reflux DECREASE in SVR

Decreased preload

Lasix/Nitroglycerin (DECREASED Preload): -when end diastolic volume decreases (preload/volume return to the heart decreases), the left ventricle empties to the previous end-systolic volume -Consequently, with decreased filling but emptying back to the previous level, stroke volume decreases (thus CO and MAP decrease) -PV loop: shorter d/t decrease pressure, thinner due to decreased volume **A decrease in pulmonary capillary wedge pressure provides evidence of the decrease in end-diastolic volume HR may reflexively increase d/t the baroreceptor reflex SVR may reflexively increase d/t the baroreceptor reflex Summary: -decreased preload -decreased EDV -decreased PCWP -ESV stays the same -decreased SV -decreased CO -decreased MAP -reflex increased HR -reflex increased SVR note: nitroglycerin decreased preload via venodilation, decreasing venous return to the heart lasix decrease preload by inhibiting sodium reabsortion in the thick ascending loop of henle, thus promoting increased water extretion

Coronary perfusion pressure

Left ventricular end-diastolic pressure and aortic diastolic pressure are the two primary determinants of coronary perfusion pressure.

Nitroglycerine

Metabolism of nitroglycerin leads to the generation of a NO molecule: -conversion of NO from nitroglycerin involves a more complex series of reactions -NO is generated from nitroglycerin enzymes in VENOUS endothelium but NOT arterial endothelium at normal doses Actions: -venodilation: decreasing preload -bronchodilation

Contractility

Myocardial contractility is the ability of the heart to generate force to a given preload and a given after load -determined by the CHEMICAL environment of the cell -examples of chemical that alter contractile function are ions (calcium [increases contractility] and magnesium), oxygen, acids, drugs, hormones -when contractility increase, the ventricle empties more completely and SV increases -when contractility decreases, the ventricle empties less completely and Stroke volume decreases inherent strength of myocyte to produce force via chemicals -independent of preload

Sinoatrial Action Potential

NO PLATEAU PHASE Resting potential (established by leaky K)= -70 mV 4: Diastole: spontaneous depolarization to threshold: a. diffusion of K out of the cell decreases b. diffusion of NA INTO CELL INCREASES PROGRESSIVELY (sodium always initiates depolarization) c. last 1/3 of phase: Ca begin to diffuse into cell 0: slow depolarization a. Sodium in b. Calcium in 3: Repolarization -K diffuses out of cell (K always initiates depolarization) 4: diastole

Decreased Afterload

Nitroprusside (dilates arterial vasculature decreasing SVR) -When after load decreases, the heart empties more completely, stroke volume increases -both end diastolic volume (preload) and end systolic volume decrease -The volume in the left ventricle decreases -there is a decrease in blood pressure -heart rate reflexively increases -ejection form the left ventricle is easier because of the decreases systemic vascular resistance so stroke volume increases -Because stroke volume (ejection) increases, the amount go blood in the left ventricle chamber decreases; the left ventricle "shrinks" and a decrease in pulmonary capillary wedge pressure provides evidence of the decrease in end-diastolic volume Summary: -afterload decreases -EDV decrease -ESV decrease -SV increases -Reflex increase HR -Bloop pressure decreases -PCWP decreases -LV volume decreases PV curve: -curve shifted to the left due to decrease in EDV & ESV -curve is shorter due to decrease in blood pressure -curve is fatter due to increase in SV side notes on nitrates and nitroprusside: -Nitrates are contraindicated in patients who have taken sildenafil within the previous 24 hours because of risk of severe hypotension. -Nitroprusside may increase intracranial pressure and therefore must be used cautiously in the treatment of hypertensive crises associated with encephalopathy.

ECG

P wave: atrial depolarization PR interval: atrial systole, AV node delay (0.12-0.2 seconds) QRS complex: ventricular depolarization (atrial repolarization) 0.12 seconds -The QRS complex results from ventricular depolarization (phase 0) -Q wave should only be 0.04 sec QT interval: ventricular systole -reflects the duration of the plateau phase (phase 2) -with hypocalcemia: QT phase prolonged -hypercalcemia: QT phase is shortened T wave: ventricular repolarization -The T wave results from ventricular depolarization U wave: not always present, present with hyperkalemia On the ECG trace, each mm corresponds to 0.04 seconds

Pacemaker AICD Cardioversion

Pacemaker: -The three letters correspond to what chamber is paced, what chamber is sensed, and whether the pacemaker is capable of inhibiting firing, triggering firing, or both. V stands for ventricle, A for atria, D for dual, 0 for neither, T for triggered, and I for inhibited. In this example (VVI), the pacemaker both senses and paces in the ventricle and is inhibited if it detects a natural depolarization. -VOO: A pacemaker that is only capable of delivering a fixed ventricular rate and does not sense spontaneous depolarizations -During the perioperative evaluation, you discover that a patient with a pacemaker occasionally experiences dizziness while exercising his chest muscles; This indicates that myopotentials may be inhibiting the pacemaker. From this information, you know that muscle fasciculations from succinylcholine should be avoided to prevent inadvertent pacemaker inhibition. AICD: Although bipolar cautery is preferred, monopolar cautery may be used in patients with an AICD as long as it is set at the lowest possible energy setting, used in short bursts, the cautery tip is kept at least six inches away from the AICD, the grounding pad is placed so that the energy flow does not pass through the AICD, and a defibrillator is available for immediate use. An AICD can be deactivated by placing a doughnut magnet over it, but this will not disable the bradycardia function of an AICD/pacemaker combo. Cardioversion: Cardioversion is the application of electrical energy to a patient to convert a cardiac rhythm such as atrial fibrillation, atrial flutter, or stable ventricular tachycardia to a normal rhythm. The electrical discharge is timed to coincide with the R wave of the QRS complex.

Paradoxical embolus

Paradoxical embolus is the transfer of an embolus from the venous system to the arterial system and often to the brain via a patent foramen ovale or atrial septal defect. -The most common defect through which this can occur is a patent foramen ovale. Autopsy studies indicate that this defect is present in about 25-35% of patients. It can also occur in other right-to-left cardiac defects such as a patent ductus arteriosus or atrial septal defect. -Normally, the transfer of an embolus is restricted because left-sided heart pressures are higher than right-sided heart pressures. Any condition that increases right heart pressures, such as pulmonary hypertension, pulmonary stenosis, or a Val Salva maneuver, can increase the chance of embolus transfer.

Arrhythmias and Treatments

Paroxysmal Atrial Tachycardia (SVTs) HR: 150-250 bpm Treatment: -vagal maneuvers such are carotid sinus massage (only applied on one side) -Verapamil (5-10 mg IV): CC Blocker, slows SA AV phase 4 depolarization- terminates AV nodal reentry successfully in about 90% of the cases and has become the DRUG OF CHOICE -esmolol: 0.5-1.0 mg/kg (50-200 mcg/kg/min infusion -propranolol: 0.5 mg IV bolus doses -Edrophonium in 5 to 10 mg IV bolus (anti cholinesterase drug: increases ACH which binds to muscarinic receptors and slows HR via parasympathetic response (shortest acting) -phenylephrine: if patient is hypotension, reflex vagal response will slow HR use 100 mcg bolus -IV Digitalis: slows heart rate by slowing phase 4 depolarization in SA and AV node: Digoxin: 0.5 to 1.0 mg IV -cardioversion SVTs: -associated with lightheadedness, dizziness, syncope, fatigue, chest discomfort -most commonly occurs due to a reentry circuit consisting of anterograde conduction over the slower AV nodal pathway and retrograde conduction over a faster accessory pathway. -It can also occur due to enhanced automaticity of secondary pacemaker cells -Polyuria may result in SVT (or any other atrial tachycardia resulting in AV dys-synchrony) due to an increased secretion of atrial natriuretic peptide due to the increased atrial pressures that result from atrial contraction against a closed AV valve PVCs: regular rhythm with occasional preventricular wide QRS complex beat Treatment: correct electrolyte abnormalities -lidocaine is usually the treatment of choice with an initially bolus dose of 1.5 mg/kg (class Ib sodium channel blocker, works on phase 4 to slow rapid depolarization in ventricular cells)

Pericarditis

Pericarditis is often due to a viral illness, but may often occur 1-3 days after a myocardial infarction. Deep inspiration worsens the pain. It is often relieved by sitting forward. The ECG changes seen in acute pericarditis occur in four stages. In stage I, there is diffuse ST segment elevation and depression of the PR segment. In stage 2, the ST and PR changes normalize. In stage 3, the T wave inverts, and in stage 4, the T waves normalize. If no other associated pericardial disease is present, acute pericarditis does not alter cardiac function. *Dresslers syndrome is a form of pericarditis seen following myocardial infarction.* *Systemic lupus erythematosus, scleroderma, rheumatoid arthritis, metastatic disease, mediastinal radiation, and various infections are all associated with an increased incidence of pericarditis *Constrictive pericarditis is similar to cardiac tamponade in many of its features. They both exhibit pulsus paradoxus and Kussmauls sign. Kussmauls sign is more common in patients with constrictive pericarditis. *Constrictive pericarditis also exhibits Freidreichs sign, which is a prominent y-descent on the central venous pressure tracing. *Acute pericarditis is associated with a friction rub on auscultation.

SA node and ventricular action potential comparison

Phase Vent Cell Nodal 0: depolarization Na in Ca in, Na in 1: transient Cl in, K out 2: plateau Ca out slow 3: repolarization K out K out 4: resting K leak K out slows Na back out K back in

Increased Afterload

Phenylphrine: Increased Afterload -When after load increases, the heart empties less completely -both end diastolic volume (preload) and end systolic volume increase -the ventricular chamber dilates d/t increase in volume that can't be pushed forward -Stroke volume (end diastolic volume - end systolic volume) decreases -blood pressure increases -left ventricle dimension increase d/t increased LV volume -ejection from the left ventricle is opposed because of the increases SVR, so stroke volume falls -HR may decrease reflexively -dec SV, dec HR = decreased CO **because SV decreases, the amount of blood in the left ventricular chamber increases including end diastolic volume therefore PCWP also INCREASES In Summary: -afterload increases -EDV increases -ESV increases -SV decreases -HR reflexively decreased -CO decreases -Bloop pressure increases -PAWP increases -LV volume increase PV cruve: -Shifts to the right due to increase in both EDV & ESV -narrows due to decreased SV -tall due to increased pressure

Left to right shunt

Positive-pressure ventilation increases pulmonary vascular resistance (PVR), which results in a decrease in the left-to-right shunt. A high FiO2 will decrease PVR and increase the shunt. Intravenous administration of neosynephrine or epinephrine will increase systemic vascular resistance which will increase the magnitude of the shunt.

Ventricular Action Potential

RESTING TRANSMEMBRANE POTENTIAL (established by leaky K) is -90 mV 4: resting membrane potential; diastole a. K diffuses slowly out of cell via leaky K channels creating a negative outer membrane. b. negatively charged proteins unable to follow K, accumulate along the inside of the cell membrane creating a INSIDE resting membrane potential of -90 mV 0: Rapid depolarization -Na channels snap open and Na diffuses into the cell creating a +30 mV action potential 1: transient brief repolarization a. Cl- leak into cell decreasing potential slightly b. K diffuses out mildly 2: Plateau Phase a. sodium channels are inactivated (another action potential cannot be fired: ABSOLUTE REFRACTORY PERIOD) b. Calcium diffuses INTO the cell slowly: maintains depolarization, delays repolarization, prolongs absolute refractory period i. hypocalcemia: QT interval is prolonged/plateau phase prolonged ii. hyper calcium: QT interval shortened/plateau phase shortened 3: Repolarization -K out of the cell responsible for repolarization (calcium ions influence the opening of the gated potassium channel for depolarization) 3-4: Sodium-Potassium pump operates to restore intra and extracellular balance

Ventricular Conduction Disturbances

Right Bundle Branch Block -wide QRS -bunny ears point right when turned 90 degrees -look at leads V1 and V6 Left Bundle Branch Block: -wide QRS -majority leads point left when turned 90 degrees -look at leads V1 and V6 -The characteristics consistent with a left bundle branch block are: QRS > 0.12 secs, lack of septal Q waves in V4-V6, I and aVL, RR' QRS pattern in I, aVL, and V4-V6, and secondary ST or T wave changes in I, aVL, and V4-V6. A deep, rounded S wave in leads I and aVL is typical of a right bundle branch block while a V5 amplitude > 26 mm is one of the characteristics of left ventricular hypertrophy

Tricuspid atresia

Right the left shunt (all T words) -Tricuspid atresia is a congenital heart defect that is characterized by a small right ventricle, enlarged left ventricle, decreased pulmonary blood flow (that occurs via a ventricular septal defect, patent ductus arteriosus, or bronchial vessels), and arterial hypoxemia. Blood passes from the right atrium to the left atrium (right-to-left shunt) via an atrial septal defect prior to ejection into the systemic circulation causing a cyanotic defect.

Leads

S: V1, V2 (Left anterior descending) A: V3, V4 (Left anterior descending) L: V5, V6, I, aVF (left circumflex) I: II, III, aVL (right coronary artery) Modified V5 lead: -V5 lead is helpful in he detection of anterolateral ischemia -to create a modified V5 lead, place the left leg and right arm leads in their normal position -then place the left arm lead over the anterior axillary line at the level of the 5th intercostal space and select Lead I as the monitoring lead

Calculations

SV = CO/HR = 60-90 ml SI = SV/Body surface areas (BSA) = 40-60 ml/m^2 SVR = (MAP -CVP)/CO x 80 = 900- 1,500 dynes sec cm-5 PVR= (PAP-PCWP)/CO x 80 = 50-150

Left Ventricle Pressure Volume Loop

Shows the relationship between ventricular pressure and ventricular volume during ONE cardiac cycle -loop begins with the opening of the mitral valve (ESV) and filling of the ventricle to the end diastolic volume -atrial kick accounts for the last 1/3 of filling pressure/volume -EDV is at point B where the Mitral Valve closes (S1 heart sound) and diastole ends and systole begins -Isovolumentric contraction at the lower right portion of the loop: pressure changes due to ventricular depolarization but volume does not change yet because all valves are closed -The aortic valve opens at the upper right portion of the loop and ventricular ejection begins (high volume to low volume to the body) -At the upper left of the loop, the aortic valve closes (S2 heart sound), systole ends, diastole begins (end systolic volume- amount of volume left in the heart after a ejection fraction) -isovolemic relaxation returns the loop to the starting point: pressure falls due to repolarization but volume stays the same because all valves are closed -Stroke volume is the difference between EDV and ESV -Diastole begins at point D and ends at point B -Systole begins at point B and ends at point D -Diastolic filling occurs between points A and B -Ejection occurs between points C and D

Pharmacology Application

SoBe PoCa (drug classes 1a, 1b, 1c, II, III, IV) Phase 4 SA AV node (Na in, Ca in) -DIGITALIS (cardiac glycoside) slows phase 4 depolarization in SA and AV nodes therefore decreasing HR -Beta Blockers: slow phase 4 depolarization -Calcium channel blockers (verapamil, diltiazem, nifedipine): slow phase 4 depolarization of SA and AV node: slow Calcium influx, slowing HR Phase 4: Ventricular Cell (Sodium influx) -Sodium Channel Blockers: suppress spontaneous phase 4 depolarization in ventricular cells--> membrane stabilizers (spontaneous depolarization during phase 4, as might occur in ischemia ventricle, is repsonsible for PVCs) Sodium Channel Blocking Classes: 1a: "Double Quarter Pounder" Disopyramide Quinidine Procainamide 1b: "Lettuce, Tomatoes, Pickles, Mayo" Lidocaine Tocainide PHENYTOIN 1b Mexiletine 1c: "Fies Please" Propafenone Flecainide (a: pro, b. phen, c. prop) Calcium channel blockers also work on phase 2 of the cardiac ventricular action potential (plateau phase)

Sodium nitroprusside

Sodium nitroprusside has NO is its configuration: -Nitroprusside is metabolized by arterial endothelial cells and venous endothelial cells to its active metabolite NO -NO is cleaved from nitroprusside at the vascular smooth wall Actions: -venodilation: decrease preload -arterial dilation: decrease afterload -bronchodilation

Cardiac Pulmonary Bypass

Standard CPB circuits are associated with dilutional anemia, inflammatory reactions, hemodilution, and coagulopathy. In order to reduce these effects, miniaturized CPB circuits have been developed.

Myocardial Ischemia and Injury

Subendocardial Ischemia: ST DEPRESSION Transmural Ischemia: ST segment ELEVATION *Obstruction of the LEFT MAIN CORONARY ARTERY is considered the most serious cardiac vessel lesion and has the least favorable prognosis despite medical treatment *the diagnosis of acute myocardial infarction requires the rise and fall in cardiac enzymes and at least one of the following: -ischemia symptoms -development of Q waves on the ECG -ECG changes indicative of ischemia -imaging data that demonstrates loss of viable myocardium Increased myocardial O2: HR > afterload > preload whatever the s/s, return the heart to a SLOW, SMALL, PERFUSED state aka: decreased HR, increase ejection/emptying (decrease PCWP, decrease after load nitroglycerin: decreased preload nitroprussside: decreased afterload beta blockers: slow heart rate *The first 30 days after an MI is associated with the highest risk for reinfarction. The mortality rate with reinfarction is 50%. Because of these statistics, it is recommended that no patient undergo elective surgery until at least 4-6 weeks after the MI. *The overall risk for a perioperative MI in the general population undergoing general anesthesia is 0.3%. *Primary myocardial dysfunction associated with coronary artery disease is the most common culprit, but valvular disease, arrythmias, and pericardial disease are also causes of left ventricular failure. *When inducing general anesthesia for a patient with chronic hypertension, you should strive to maintain the mean arterial blood pressure within 20 percent of normal.

Idiopathic hypertrophic subaortic stenosis (IHSS) Hypertrophic Cardiac Myopathy

The P-V lopp in IHSS is shifted to smaller volumes and larger pressures (due to outflow tract obstruction -only IHSS causes this type of combined shift -Hypertrophic cardiomyopathy involves enlargement of the interventricular septum (excess muscle growth on septum) which results in left ventricular outflow narrowing --> ASSYMETRIC SEPTAL HYPERTROPHY (ASH) -ALSO, Mitral Regurgitation, leaflet swings open and blocks aortic outflow in late systole (outflow tract obstruction), this phenomenon is caused by the Venturi effect (narrowing causes entrainment effect) -->>> SYSTOLIC ANTERIOR MOTION of the Mitral valve (SAM) Management: -HR: maintain HR (not too slow, not too fast) -Rhythm: keep in NSR (may see Afib due to dilation of the left atrium) -Preload: INCREASE (volume is the first defense for hypotension; must keep preload FULL to help keep blood pressure stable -Afterload: INCREASE (pure vasoconstrictor is the 2nd like of defense for hypotension_ -Contractility: DECREASES Pathophysiology: -Diastolic dysfunction is reflected by elevated LV end diastolic pressure -Diastolic stiffens is due to an abnormal hypertrophied intraventricular septal muscle below the aortic valve, which blocks outward flow during during systole (the subaortic area is narrowed, contributing to outflow obstruction as well -venturi effect draws leaflets out as blood rushes by --Bernoulli -There will be left ventricle hypertrophy as well, deep broad Q waves -RESULTS: obstruction in mid to late diastole Obstruction INCREASES or DECREASES: Old Cats Pea A lot Obstruction: increase decrease Contractility: increase decrease Preload: decrease increase Afterload: decrease increase -This obstruction is worsened by increased heart rate or increased myocardial contractility as well as decreases in preload or afterload. -Anesthesia is usually maintained by controlled myocardial depression using volatile anesthetics. -most common result in sudden cardiac death in people under 30 Dysrhythmias result in disorganized cellular architecture, myocardial scarring, and expanded interstitial matrix and are associated with risk of sudden death AICD are common in this population; bring in external debit with pads on patient if using bovie ; magnet defaults to assynchronis rhythm s/s: -fatigue or syncope -angina pectoris, relieved by lying down -dyspnea on exertion -tachydysrhythmias (both SVT and ventricular arrhythmias are common) -heart failure Diagnosis: -ECG exhibits left ventricle hypertrophy, ST wave abnormalities, Q waves, left ventricle enlargement (ECHO) -cardiac catheterization will directly meausre the increased LVDP and LVOT pressure gradient Treatment: -Beta blockers and calcium channel blockers decrease contractility and prevent increases in subaortic pressure gradients -calcium channel blockers may improve diastolic relaxation -Nitrates, digoxin, and diuretics worsen LV obstruction (want increase preload and after load) Anesthesia considerations: 1. Look for: dynamic obstruction, malignant arrhythmias, myocardial ischemia 2. Goals: minimize sympathetic activiation which will increase contractility, avoid hypovolemia, minimize decreases in left ventricular after load, minimize left ventricle outflow tract obstruction 3. Arterial waveform may be bifid (bisferiens pulse) 4. NO CENTRAL NERVE BLOCKS--> will decrease preload and after load 5. Regional anesthesia may exacerbate left ventricle outflow obstruction by decreasing both cardiac preload and after load 6. Phenylephrine and other pure alpha agonists are ideal vasopressors because they do not augment contractility, but increase SVR 7. Beta adrenergic agonists will counter the effects of sympathetic activation and decrease obstruction 8. Altered coronary perfusion ill exist with LV hypertrophy because the decreased myocardial blood supply and increased myocardial oxygen demand causes altered coronary perfusion Most common genetic cardiovascular disesse affects all ages, and have autosomal dominant inheritance

Arterial Pressure Waveforms

The pulse pressure increases as the arterial pressure waveform passes into more peripheral arterial vessels; thus pulse pressure is greatest in the dorsalis pedis -The increase in pulse pressure as the pressure wave moves more peripherally is attributed to an increase in SBP and a decrease in DBP -The SUPERIMPOSITION principle explains this phenomenon The most accurate measures of arterial blood pressure is taken from the area under the aortic pressure curve -the area under there arterial curve divided by time yields MAP

Preload

The tension (force) present in the wall of the LV at end-diastole (immediately prior to contraction) -preload is determined by the VOLUME of blood in the left ventricle chamber at end-diastole -the greater the filling, the greater the preload. -When preload increases, SV increases Determined by: -intravascular volume: determined by the amount of sodium in the body = amount = aldosterone) -venous tone (return of blood to heart; veins have smooth muscle that response to sympathetic stimulation) - ventricular compliance (increase compliance = more volume) CVP = right sided preload LVEDV/PAWP= left sided preload Frank-Starling Law: the more you fill the heart, the more it will pump forward

Cardiac Markers

Troponin is a cardiac specific marker for myocardial infarction that becomes elevated within 3 hours of myocardial injury and remains elevated for several days following the event

Unstable Angina

Unstable angina is characterized by: -substernal chest pain that began less than 2 months ago -has progressively increased in severity, duration, or frequency -less responsive to pharmacologic therapy -occurs at rest -lasts longer than half an hour -exhibits transient T-wave or ST segment changes.

Ventricle Septal Defect

Ventricular septal defects are the most common congenital heart defect in infants and children

Mitral Stenosis

With mitral stenosis, left ventricle filling is diminished -the PV loop reflects a decreased preload (EDV) reduced filling but empties to the same extent -both isovolumetric contraction and relaxation are normal (straight lines) -Mitral stenosis is a mechanical obstruction to left ventricular diastolic filling due to a decrease in the size of the mitral valve orifice. -It is most commonly caused by rheumatic heart disease, but may also result from carcinoid syndrome, left atrial myxoma, rheumatoid arthritis, lupus, or thrombus formation. -It results in an increase in left atrial volume and pressure. -An increase in left atrial pressure usually maintains stroke volume, but it may decrease with tachycardia or loss of atrial contraction -left atrium dilates (pressure) and if mean pulmonary artery capillary pressure goes > 25 mmHg, PVR increases -right ventricle failure is precipitated by acute or chronic elevation in right ventricle after load -90% of patients present with CHF and a fib -a fib promotes clot formation in the left atrial chamber (go to head) -hemoptysis -overt pulmonary edema -10-15% develop chest pain -enlarge atrium may apply pressure to left RLN and cause hoarseness Management: HR: lower Rhythm: NSR Preload: maintain Afterload: maintain (avoid decrease in SVR and increase in PVR) Contractility: maintain MV area: 4-6 cm^2 Mitral stenosis < 2 etiology: -delay complication of acute rheumatic fever -2:1 female -stenosis begins 2 years following acute disease and results from progressive fusion and calcification of the valve leaflets Treatment: -diuretics -heart rate control -anticoagulation -surgical correction -MS pts are sensitive to the vasodilation actions of central blocks, epidural is preferred -control a fib rate with diltiazem or digoxin -phenylephrine -PROMINENT A WAVE ON PCWP Heart sounds: an opening snap in early diastole, a rumbling diastolic murmor at apex or axilla EMBOLIC EVENTS AND AFIB *A mean left atrial pressure of 25 mmHg is required when the mitral area is less than 1 cm2. If this pressure is sustained, the patient will likely develop pulmonary hypertension.