CCRN Cardiac

Papillary muscle rupture

2-7 days after MI Causes acute mitral regurgitation in left side causing pulm edema, hypotension, systolic murmur Diagnose with ECHO Urgent surgery needed

RA pressure

2-8 mmHg Same as CVP

RV pressure

20-25/6-12

SVR

AFTERLOAD of left ventricle Normal is 700-1500

S4

Caused by atrial contraction of blood into a noncompliant ventricle Occurs right before S1 Best heard at apex of heart with bell Associated with myocardial ischemia, infarction, hypertension, ventricular hypertrophy, and *aortic stenosis*

Nesiritide (Natrecor)

Endogenous BNP; vasodilation/natriuresis

ECG

Ischemia: ST segment depression Injury: ST segment elevation Infarction: Q waves -take about 6-8 hrs after ischemia starts to form because that is the full thickness of the muscle. Can be a sign of an old MI because they never go away

Aortic valve

LV preload increased; LV stretches out and has to work harder Stenosis: systolic murmur. Will have a fixed CO - aorta can only let a certain amount through. *Vasodilation and reduced preload is dangerous*. Can be replaced surgically or transvascular. Regurgitation: Blood backs into LV. Diastolic murmur

acute coronary syndrome

sudden symptoms of insufficient blood supply to the heart indicating unstable angina or acute myocardial infarction. Usually caused by plaque detaching from the vessel wall and biggest risk is arrhythmias. Does NOT include stable angina

Systemic Vascular Resistance (SVR)

the pressure in the peripheral blood vessels that the heart must overcome to pump blood into the system; afterload; normal 800-1200

Labetalol

Alpha and beta blocker

Nicardipine

CCB; more vasodilator effect. Longer half-life 15-45 min

Treatment of STEMI

Determine onset of infarct. If onset <12 hours, REPERFUSION with PCI (door to balloon 90 min) or fibrinolytic therapy (door to drug <30 min) Eligibility criteria: ST elevation in 2 or more contiguous leads or new onset of LBBB, onset of chest pain <12 hours, chest pain of 30 min in duration, chest pain unresponsive to sublingual NTG

S1

Loudest at apex of heart Marks end of diastole, beginning of systole

Anterior leads

VI-V4 Look at front of heart

Preload

the volume of blood either in the right atrium or in the left ventricle at the end of diastole or the beginning of systole. Preload is quantified with central venous pressure (CVP) and pulmonary artery occlusive pressure (PAOP), respectively; these parameters reflect a patient's volume status. The end-diastolic volume (EDV) is related to the amount of stretch of the sarcomeres. Preload is a reflection of all of the elements that affect tension of the chamber wall at the end of filling (diastole). Insufficient preload results in decreased stroke volume causing compensatory increase in heart rate to maintain CO. Increased HR increases o2 demand Excess preload causes tension on the ventricular wall resulting in compression of the smaller blood vessels resulting in decreased o2 delivery

Second degree heart block type I

- aka Wenckebach - typically stable - *progressiveley prolonged PR interval WITH QRS DROP* - unique feature is presence of a *prolonging PR interval from one cardiac complex to the next until it reaches a point where the QRS complex is blocked or missing* - *p-p intervals are regular and r-r intervals are irregular* Heart blocks do not typically respond to atropine!!! Must pace if unstable

Drugs that prolong QT interval

- antiarrhythmics (amiodarone, lidocaine, procainamide) - ABX (quinolones, macrolides) - azole antifungals - antidepressants (tricyclics, SSRI's, SNRI's, mirtazapine, trazodone) - antiemetic agents (5HT3 antagonist, droperidol, phenothiazines) - antipsychotics (aripiprazole, asenapine, chlorpromazine, clozapine, *haloperidol*, iloperidone, *olanzapine*, paliperidone, pimozide, *quetiapine*, risperidone, thioridazine, ziprasidone) - oncology agents (arsenic, -nib) - PI's (atazanavir, saquinavir), rilpirvirine - anesthesics (propofol, sevoflurane) - anti-malarials (chloroquine, quinine) - bladdar (Mybertiq, Vesicare, alfuzosin) - Pain (methadone, buprenorphine) - PK/AD (apomorphine, donepezil, galantamine) - anti-cholinergic agents (benadryl, tizanidine) - others (Strattera, Fingolimod, Pentamidine, Ranexa, Tacrolimus) *hypokalemia, hypocalcemia, hypomagnesemia*

MI and murmurs

-Mitral valve is attached to the left ventricular wall by the papillary muscles and chordae tendinae. Ischemia or infarction can affect mitral valve function and lead to acute mitral valve regurgitation -Papillary muscle dysfunction is loudest at apex -Papillary muscle rupture loudest at apex and surgical emergency -Ventricular septal defect *sternal border* 5th ICS

Calcium channel blockers

-dipine CCBs are not routinely prescribed for patients with ACS. Howver, they are useful in patients who are intolerant of beta blockers and those with vasospastic disease and hypertension, since they *block vascular smooth constriction and can decrease heart rate*. Used in diastolic heart failure

ACE inhibitors

-prils Beneficial for patients with heart failure with low EF, large anterior MIs or pulmonary congestion in absence of hypoxia, or stable CKD. ACE inhibitors prevent remodeling of myocardium and decrease preload/afterload, decreasing workload of heart. Contraindicated in patients with history of bilateral renal artery stenosis. Can cause hyperkalemia

Angiotensin receptor blockers

-sartan Some patients do not tolerate ACE inhibitors since they prevent the breakdown of bradykinin, causing a dry, hacking cough. These patients take ARBs instead with similar results Can cause hyperkalemia

PVR

AFTERLOAD of right ventricle Normal is 20-130

Phenylephrine

Alpha 1 receptor agonist ONLY that causes arterial constriction, increasing afterload without associated change in HR. May decrease CO due to increased afterload (minimal effect on beta receptors of heart) Precautions: extreme caution in those with partial cardiac block, bradycardia, severe atherosclerosis, and myocardial disease. May cause severe bradycardia. Increased risk of ventricular arrhythmias or MI in elderly patients

Carvedilol

Alpha and beta blocker

Giapreza

Angiotensin II - causes vasoconstriction and increases fluid retention. Use as secondary vasopressor. Need VTE prophylaxis because of increased risk for thromboembolic events

ARNIs

Angiotensin receptor neprilysin inhibitors Used in conjunction with valsartan to improve HF. Inhibits breakdown of naturally occuring natriuretic peptides, resulting in an increase in circulating endogenous peptides, which promotes natriuresis, diuresis, and vasodilation Adverse effect include hypotension, hyperkalemia, and angioedema

Amiodarone

Antiarrhythmic drug that lengthens cardiac action potential and blocks myocardial potassium channels leading to slowed conduction and prolonged refractoriness. Also blocks sodium channels, has anti-sympathetic properties, and negative inotropic properties Precautions: greater toxicity in elderly. Can cause v-tach, increased resistance to cardioversion, and Torsades. Bradycardia Pulmonary fibrosis is a long-term complication of oral amiodarone. IV amio can also cause acute liver failure. Amio may prolong QT interval. Also contains organic iodide, which can result in thyrotoxicosis or amio-induced hypothyroidism

Aortic dissection

Aorta breaks and blood leaks into false lumen between media layer and adventitia layer Risk factors: hypertension (70-90%), something that causes weak vessel allowing a tear (trauma, genetic, Marfans) Most dissections happen in the arch where there is more pressure Symptoms: end-organ ischemia, MI, pericardial effusion or tamponade. Sudden, severe pain in chest, flank, or epigastric. Spasm occurs which makes them hypertensive until they lose enough blood and they become hypotensive. Acute aortic insufficiency possible - diastolic murmur and audible S4. Pulseless extremity or higher BP in one arm is a sign. Descending usually characterized by pain in back, shoulder blades, abdomen, or legs Diagnostics: CXR showing wide mediastinum. ECG may show LVH or AMI. CT with contrast/angiogram. TEE (ascending) vs. TTE (descending) depending on location of dissection. MRI. Treatment: BP management - lower as soon as possible with beta blockers (esmolol, labetalol) and vasodilators (nipride, nicardipine - do not use until after you control HRbecausewillcausereflextachycardia) Ascending: surgical intervention immediately Descending: repair can cause acute renal failure or paralysis from clamping aorta. Need to monitor spinal pressure with lumbar drain afterwards. Ongoing BP control after repairs

MI complications

Arrhythmias most common Defib VF Drug therapy for stable, sustained VT and to prevent recurrent VF (procainamide, amio, sotalol) Synchronized cardioversion for unstable, sustained VT Bradycardia, heart blocks, sick sinus syndrome A-fib - 10-15% of all MIs, have increased mortality, even when returned to NSR Heart failure Cardiogenic shock Re-infarction Thromboembolic events Pericarditis (Dressler's syndrome) Ventricular aneurysm Ventricular septal defect Papillary muscle rupture Cardiac wall rupture

Anterior MI

Associated with left anterior descending occlusion ST elevation in V1-V4 Reciprocal changes in inferior wall (ST depression) in II, III, aVF May develop 2nd degree type II or RBBB (*LAD* supplies bundle of HIS) - not a good sign, and ventricular dysrhythmias Development of systolic murmur - possible ventricular septal defect Higher mortality than inferior - HEART FAILURE

Mitral valve

Between LA and LV Stenosis: LA has to work hard to get blood to LV - blood backs up to lungs and LA. May have AF d/t stretch of LA. Risk for LA thrombus with or w/o AF. Murmur during diastole. PAOP will be falsely elevated because not true reflection of ventricular pressure. Regurgitation: blood goes backwards into LA and LV hypertrophies to create CO. Murmur during systole. Both cause dyspnea and pulm symptoms/AF Management: treat hemodynamics, repair valve. May need to be on anticoagulation with new valve

Beta blockers

Block sympathetic nervous system stimulation at beta receptors. Decrease afterload by causing arterial vasodilation. Slow the heart rate to allow increased diastolic perfusion time, increasing blood flow and oxygen supply to coronary arteries. Decrease contractility, which decreases myocardial oxygen demand. Decreases the incidence of ventricular dysrhythmias. Prevent ventricular remodeling, retaining a more normal systolic function. Contraindications include SBP <90, cardiogenic shock, severe bradycardia, second or third-degree AV block, or heart failure on presentation

CVP

Blood pressure in vena cava/right atrium. Reflects RV function/preload and venous return to right side of heart PRELOAD of right atrium Low indicates hypovolemia, high indicates RV failure, pulm HTN, PE, tamponade, constrictive pericarditis Normal 2-6 mmHg

CO/CI

CO = HR x SV Normal 4-8 L/min Larger people have larger COs CI corrects for body surface area Normal 2.6-4.2

Clevidipine

Calcium channel blocker that decreases MAP by decreasing SVR without reducing cardiac filling pressure or increasing HR Precautions: may exacerbate HF due to negative inotropic effects. Hypotension and reflex tachycardia may occur.

Structural heart defects

Can be genetic, from HF, cardiomyopathy, aging, infection. AV septal defect from MI or genetic

Friction rubs

Can be pericardial or pleural

Clinical patterns

Cardiogenic shock: PAOP elevated, CI low, SVR elevated Hypovolemic shock: PAOP low, CI low, SVR elevated Septic shock (early): CI elevated, SVR low, PVR elevated RV failure: CVP elevated, CVP > PAOP, CI low Tricuspid regurgitation: CVP elevated, RVEDP elevated Acute mitral regurgitation: elevated PAOP Acute PE: CO low, PA high, PVR high, PAOP normal Chronic pulm HTN: CVP high, RV systolic high, PA high, PVR high, PAOP normal Tamponade: CVP = PAOP elevated, CI low

Epinephrine

Catecholamine that acts on ALL alpha and beta receptors. Most potent alpha receptor activator. Causes vasoconstriction (alpha) and also induces relaxation of bronchial smooth muscle by acting on beta receptors. Precautions: large doses can cause sharp rise in blood pressure that may lead to cerebral hemorrhage. Risk of precipitating angina and infarction and/or inducing ventricular arrhythmias in patients with preexisting hypertension or cardiac disease, and those taking meds that may sensitize the heart to arrhythmias.

Balloon angioplasty

Catheter tip is advanced over a guidewire into the coronary artery intil the balloon is positioned across the atherosclerotic lesion. Balloon is inflated, resulting in fracture and compression of the atherosclerotic plaque. This stretches the coronary artery and breaks up any clots that may have formed on lesion. Is used in MI and angina patients.

S3

Caused by rapid rush of blood into dilated ventricle Occurs early in diastole, right after S2 Heard best at apex with bell Associated with heart failure, pulmonary hypertension, cor pulmonale, mitral/aortic/tricuspid insufficiency

High lateral LV

Changes in I, aVL

RCA, inferior LV

Changes in II, III, aVF Inferior MI - supplies SA node, AV node

RCA, posterior LV

Changes in V1, V2

Left anterior descending, anterior LV

Changes in V1, V2, V3, V4 Anterior MI - supplies bundle of His

RCA, RV infarct

Changes in V3R, V4R

Low lateral LV

Changes in V5, V6

Circumflex, lateral LV

Changes in V5, V6, I, aVL

Unstable angina

Chest pain at rest, unpredictable, may be relieved with NTG, troponin negative, ST depression, or T-wave inversion on the ECG

Stable angina

Chest pain with activity, predictable, lesions usually fixed and calcified lesions

Fibrinolytic therapy

Contraindications: any prior intracranial hemorrhage, known AV malformation, known malignant intracranial neoplasm, ischemic stroke within 3 months EXCEPT acute ischemic stroke within 3 hours, suspected aortic dissection, active bleeding or bleeding diathesis (excluding menses), significant closed-head or facial trauma within 3 months. Need to bring BP down <180 before adminstering Evidence of reperfusion: chest pain relief, resolution of ST segment deviations, marked elevation of troponin/CK-MB due to myocardial "stunning" when vessel opens, reperfusion arrhythmias (VT, VF, accelerated idioventricular rhythm) due to myocardial "stunning" Nursing management: assess for major and minor bleeding, change in LOC, bleeding precautions, assess for reperfusion and re-occlusion

Cardiac catheterization

Diagnostic vs interventional (balloon or stent) Preprocedure: screening and education Access sites: left heart cath - radial, femoral, brachial. right heart cath - femoral, IJ

Nitroprusside

Dilates both arterioles and veins, resulting in decreased preload and afterload. This might be used in combination with dobutamine or dopamine in cardiogenic shock until an IABP can be placed. Cyanide toxicity possible if using >48 hrs

PAOP/PAWP

Estimates left atrial pressure. Insert balloon into small pulmonary artery. Reflects PRELOAD of left heart. PAOP value will be close to the diastolic volume of PAP. Always measure at the end of expiration. In spontaneous ventilation, pressure will go UP during exhalation. In mechanical ventilation, pressure will go DOWN during exhalation Low indicates hypovolemia, RV failure, PE High indicates LV failure, hypertension, constrictive pericarditis 6-12 mmHg

Hypertensive urgency

Goal is to lower BP in 24-48 hours - oral agents adequate. ACE inhibitors, CCBs, alpha-2 stimulators (clonidine)

Hypertensive emergency

Hypertensive emergency is elevated BP with evidence of end-organ damage (brain, heart, kidney, retina) that can be related to acute HTN --> need critical care admission Hypertensive CRISIS is elevated BP without evidence of end-organ damage --> usually no need for critical care admission Causes: many factors, something leading to abrupt vasoconstriction causing endothelial damage and platelet activation. Also causes release of chemical mediators. Kidneys get damaged leading to pressure natriuresis. This causes decreased volume, which causes more vasoconstriction Treatment for hypertensive emergency or crisis: reduce MAP by 25% in first 2 hours - controlled, predictable, and safe fashion. Do not want to cause cerebral hypoperfusion. Treat with IV vasodilators, CCBs, or beta blockers -Nitroprusside: preload and afterload reducer. Assess for cyanide toxicity secondary to drug metabolite: mental status change (restless, lethargic), tachycardia, seizures, need for increase in dose, unexplained metabolic acidosis, especially in those with renal impairment or when drug is used >48 hours -Labetalol: intermittent IV doses preferred to continuous infusion due to possibility of continuing of drug beyond max dose of 300 mg. Duration of effect persists 4-6 hours after IV dose is DC'd Biggest risk is STROKE

High lateral leads

I, aVL

Inferior leads

II, III, aVF Look at bottom of heart

Dopamine

Immediate precursor of norepinephrine. Low doses (5 mcg/kg/min) have *beta adrenergic receptor activation*, increasing contractility and HR, and leading to increased CO and variable SVR. May increase myocardial oxygen demand. Higher doses have minimal beta effects and alpha effects are predominate, resulting in *vasoconstriction* and increased SVR. Higher doses contraindicated in ACS Precautions: ventricular arrhythmias. Hypotension may occur at lower infusion rates

CABG

Indications: left main coronary artery occlusion, disease in 3 or more coronary arteries Take an artery from somewhere else and reroute blood around the blockage in the coronary artery Post-op care: maintain hemodynamics with volume status and pacing; maintain adequate ventilation/oxygenation - atelectasis and pleural effusions can be common (ambulate). Expect hypotension as the patient rewarms from bypass because they will vasodilate. Monitor for complications: bleeding, tamponade, infection (pericarditis) dysrhythmias, recurrent ischemia, stroke Nursing concerns: pain, immobility, sternal precautions, lifestyle modifications, nutrition, medical therapy

S2

Loudest at base of heart (2nd ICS right sternal border) Marks end of systole, beginning of diastole S2 splits on inspiration (wide fixed splitting of S2 caused by RBBB) S2 louder with pulmonary embolism

Heart sounds

Lub-dub Lub - AV valves close Dub - aortic and pulmonary valves close

Diastolic murmurs

Lub-dub-shhhhb Heard during diastole During diastole, semilunar valves are CLOSED -Aortic insufficiency; pulmonic insufficiency During diastole, AV valves are OPEN -Mitral stenosis; tricuspid stenosis Mitral stenosis is associated with a-fib due to atrial enlargement that occurs over time

Systolic murmurs

Lub-shhhhb-dub Heard during systole During systole, semilunar valves are OPEN: -Aortic stenosis; pulmonic stenosis During systole, AV valves are CLOSED: -Mitral insufficiency; tricuspid insufficiency Mitral insufficiency will cause large giant V-waves on the pulmonary artery occlusive pressure tracing if patient has PA catheter Ventricular septal defect, which is common with acute anterior MI, may result in systolic murmur. It is heard at the left sternal border, 5th ICS

PCI

Monitor for signs of reocclusion: chest pain, ST elevation --> contact physician Monitor for vasovagal reactions during sheath removal --> give fluids/atropine. Signs include hypotension <90 with or without bradycardia, absence of compensatory tachycardia, pallor, nausea, yawning, diaphoresis Monitor for bleeding at sheath site --> immediately apply manual pressure 2 finger breadths above sheath site. Continue for 20-30 min to achieve hemostasis Monitor for retroperitoneal bleeding --> fluids/blood products. Signs include sudden hypotension, severe low back pain. Monitor for vascular complications - pulse assessments Femoral access - needs to lie flat for 2-6 hours Complications of PCI: Death is rare Coronary artery perforation, distal coronary artery embolization, intramural hematoma, failure of stent deployment *Stent thrombosis* - most incidents occur acutely within 24 hours of stent placement or subacutely within first 30 days Stroke or TIA: greater risk if with aortic stenosis Arrhythmias Renal failure *Retroperitoneal bleed* Contrast induced nephropathy: prevent with preprocedure hydration

Insufficiency vs stenosis

Murmurs of insufficiency (regurgitation) occur when the valve is CLOSED. Can be chronic or acute Murmurs of stenosis occur when the valve is OPEN. Always chronic

Oxygen demand/supply

Must increase supply and lower demand in order to prevent ischemia. Increase supply of O2 by applying O2 and increasing coronary perfusion Lower demand of O2 by decreasing preload and afterload, while improving contractility and HR

Treatment of NSTEMI

NO emergent reperfusion - same meds as STEMI. Statin therapy should be initiated. If high risk or continued chest pain, signs of instability, start GP IIb/IIIa inhibitors and prepare for diagnostic cardiac cath within 4-24 hours

Second degree heart block type II

PR intervals remain constant and QRS's are dropped - there will be more P waves than QRS's Heart blocks do not typically respond to atropine!!! Must pace if unstable

LVEDP

PRELOAD of left ventricle. Roughly equivalent to the PAOP 6-12 mmHg

Dobutamine

Potent inotrope that stimulates beta receptors of heart with moderate vasodilator properties, increasing contractility and decreasing afterload without significant increase in HR. Indicated for acute decompensated heart failure and cardiogenic shock Use cautiously because increases myocardial oxygen demand and can cause hypotension and ventricular dysrhythmias Precautions: marked increase in HR and BP should be expected. Patients with a-fib at risk for developing rapid ventricular response

PAP

Pressure in pulmonary artery May be measured during right heart catheterization or introduction of a catheter into the pulmonary artery AFTERLOAD of right ventricle Normal 20-25/4-8

RVMI treatment

Problem with RVMI is decreased preload to left ventricle. This causes decreased stroke volume and CO. Avoid nitrates, beta blockers, vasodilators, and diuretics that decrease preload. *Treat with fluids and inotropes such as dobutamine* to help ventricular output. May need to pace due to possibility of infarct in AV nodes causing heart blocks. Most likely will not respond to atropine

Patient care during sheath removal

Record baseline peripheral pulses and vitals Pain management before removal Monitor BP q 5-10 min during removal Monitor for vasovagal response. If it occurs, hold nitrates, give atropine 0.5 mg IV (even in absence of bradycardia if other signs occur), IV bolus 250 mL NS if not immediately responsive to atropine Assess for anxiety/pain as attributing factors Achieve hemostasis - manual pressure for 20-30 min, mechanical clamp compression using fem-stop or C-clamp, closure device

Inferior MI

ST elevation in II, III, aVF (inFerior) Reciprocal changes in lateral wall (ST depression): I, aVL *Right coronary artery* infarct Associated with AV conduction disturbances: 2nd degree type I, 3rd degree, sick sinus syndrome, sinus brady - be prepared to pace Development of systolic murmur: mitral valve regurgitation secondary to papillary muscle rupture Tachycardia associated with inferior MI --> higher mortality Also associated with RV infarct and posterior MI Use beta blockers and NTG with CAUTION

Lateral MI

ST elevation in V5, V6 (low lateral) ST elevation in I, aVL (high lateral) Generally involves left circumflex artery Supplies AV node with blood and lateral wall of left ventricle Can have heart blocks Often associated with anterior or inferior wall MIs

Management of acute chest pain

STAT ECG, done and read within 10 min Anti-ischemia: NTG, morphine (vasodilates and treats pain), oxygen (if hypoxic), beta-blocker (caution because at risk for cardiogenic shock) Want to give *two* antiplatelet agents: ASA and other Aspirin - chew, give ASAP Anticoagulant: heparin or lovenox Antiplatelet agents: clopidogrel, abciximab, eptifibatide, tirofiban Beta blocker: unless ACS caused by cocaine. Use cardioselective such as metoprolol, do not use propanolol. Contraindications include hypotension, bradycardia, use of Viagra Treat pain: NTG or morphine History, risk factor assessment: labs, cardiac biomarkers, CBC, lipid profile, electrolytes, BUN, creatinine, magnesium, PT, PTT

Aortic aneurysms

Sac forms in wall of aorta Risk factors include aging Complications: aneurysm rupture or clot formation Repair indicated for any aneurysm causing symptoms or risky aneurysms>5.5cm Priority is to keep from rupturing by controlling BP. Post op care: keep BP controlled and watch for AKI Abdominal aortic aneurysm can be repaired with open surgery and EVAR. EVAR: endovascular aneurysm repair. Does not remove sac, but stent stays open in aorta and blood flows through stent instead of aneurysm. No aortic clamping, but high risk for renal injury r/t contrast use. Monitor sites and peripheral pulses

Esmolol and metoprolol

Selective beta-1 blocker

Nitroglycerin

Smooth muscle vasodilation in *coronary arteries*, reducing preload and afterload and O2 demand. Low dose primary effect is preload reduction through *venous* dilation, while high dose primary effect is *arterial* dilation, slightly reducing afterload. Contraindicated with SBP <90 or drop >30 from baseline, marked bradycardia or tachycardia, took a phosphodiesterase inhibitor within 48 hours, suspected of having a right ventricular infarct, or hypotension secondary to nitrates that prevents adminsitration of beta blockers

Aldosterone antagonists

Spironolactone and eplerenone. Used with ACE-I or ARBs and a beta blocker to improve mortality in HF.Potassiumsparing

Valve replacement or repair

Surgical repair: incision to relieve stenosis or repair tears/chordae tendinae. Can use mechanical or bio valve Transcatheter repair: mitral valve can be clipped or stenotic valves can be opened with balloon angioplasty. Or TAVR Complications: must maintain preload while heart gets used to new valve because used to having increased volumes. Watch for arrhythmias and heart blocks due to valves being close to nodes (may need temp or permanent pacemaker). Anticoagulation usually necessary - direct oral anticoagulants (riviroxiban, apixaban) are contraindicated with mechanical valves Tissue valves often require anticoagulation temporarily, whereas mechanical valves require more longterm anticoagulation Aortic valve replacement: may develop AV block d/t edema, inflammation, or hemorrhage near the node

Vasopressin

Synthetic of hormone vasopressin, which causes constriction of smooth muscle via V1 receptors, which stimulate the release of vasoconstrictive calcium. Can also have antidiuretic properties. Precautions: cardiac output may worsen if used in patients with impaired cardiac response. Adverse effects: A-fib, cardiac arrest, right ventricular failure, *myocardial ischemia*, pulmonary edema

Pulse pressure

Systolic pressure - diastolic pressure = pulse pressure Normal is 40-60 Systolic pressure is indirect measurement of CO and SV Diastolic pressure is indirect measurement of SVR Narrow pulse pressure (100/78) seen most in hypovolemia or severe drop in CO Widening pulse pressure (100/38) indicates vasodilation, drop in SVR, septic shock Diastole is normally 1/3 longer than systole Coronary arteries perfused during diastole

Effects of hypertensive emergency

TIA, stroke, retinopathy, signs of HF, dysrhythmias, MI, pulm edema, blood in urine (kidney damage)

Right ventricular infarct

The right coronary artery, which supplies the inferior wall of the left ventricle, also supplies the right ventricle. Therefore, about 30% of inferior wall MI patients also have a RV infarct Jugular venous distension, high CVP, hypotension, clear lungs, bradyarrhythmia ST segment elevation in inferior leads on right-sided EKG Treatment: IV fluids to increase preload, positive inotropes Avoid preload reducers such as nitrates and diuretics because it will further reduce LV filling (preload) and cardiac output. Caution with beta blockers due to hypotension

NSTEMI

Troponin positive, ST depression, T-wave inversion, unrelenting chest pain

STEMI

Troponin positive, ST elevation in 2 or more contiguous leads, unrelenting chest pain

Biochemical cardiac markers

Troponins - rise 2-5 hours; peak 24-48 hrs; normal 5-14 days CK-MB - rise 4-6 hours; peak 12-24 hours; normal 2-3 days. less sensitive than troponin; can be skewed by skeletal muscle damage

Thoracic dissections

Type I: originates in the ascending aorta, and propagates at least to the aortic arch and often beyond distally to descending Type II: originates in and is confined to ascending aorta Type III: originates in the descending aorta, rarely extends proximally

Variant or Prinzmetal's Angina

Unstable angina associated with transient ST segment elevation Due to coronary artery spasm with or without atherosclerotic lesions Occurs at rest, may be cyclic (same time each day) May be precipitated by nicotine, ETOH, cocaine Troponin negative NTG administration results in relief of chest pain, STs return to normal

Hydralazine

Vasodilator

Enalaprilat

Vasotec ACE inhibitor that causes vasodilation and decreases SVR

Norepinephrine

Works on alpha-adrenergic receptors AND beta-adrenergic receptors. Causes peripheral vasoconstriction and inotropic stimulation of the heart and coronary artery vasodilation. No specific contraindications Adverse effects: bradyarrythmia, hypertension, cardiac dysrhythmia, extravasation

Digoxin

cardiac glycoside Can be used in a fib to supplement for atrial "kick" Do NOT use cardioversion if digoxin toxicity is present - will cause VT or VF

Valvular heart disease

disorders involving valves of the heart that impact the heart's ability to pump blood effectively to the lungs or tissues of the body and cause the heart to work harder Can be caused by CAD, ischemia, acute MI, dilated cardiomyopathy, degeneration, bicuspid aortic valve (genetic), rheumatic fever, infection, connective tissue diseases

Cardiac output

heart rate x stroke volume; normal 4-8 L/min

Ventricular septal defect

large hole between two ventricles lets venous blood pass from the right to the left ventricle and out to the aorta without oxygenation. Will see an increase in RV oxygenation due to blood passing through from the LV

Milrinone

phosphodiesterase inhibitor - properties similar to dobutamine. Will cause increased contractility by raising intracellular ionized calcium and decreased afterload without increasing HR. Also causes peripheral vasodilation. Should result in a decrease in PAP, PAOP, and SVR May require concomitant vasopressor administration to keep sufficient MAP Precautions: ventricular and supreventricular tachyarrythmias. Administration should not exceed 48 hours d/t increased risk for arrhythmias. Obstruction may be aggravated in patients with severe obstructive pulmonic or aortic valvular disease. Acute phase post MI not recommended. Use with diuretics can cause decreased filling pressure Increases contractility and vasodilates