Ch.16 - Ischemic heart disease and conduction disorders

Heart layers + coronary arteries

• epicardium - outer layer

• myocardium - muscle layer

• endocardium - lines interior layer

Left coronary artery common for MI

Exercise increases coronary collateral vessels AKA hypertrophy

Chambers of the heart

4 chambers

• Right atrium: receives blood from superior and inferior vena cava and coronary sinus

• Right ventricle: pumps blood into lungs via pulmonary artery

• Left atrium: receives blood from pulmonary veins

• Left ventricle: pumps blood to body via systemic arteries

Pulmonary vs. Systemic circuit

Pulmonary circuit

• low pressure system because only between heart and lungs

• RV pumps deoxygenated blood to lungs, blood picks up oxygen in lungs, returns to LA

Systemic

• high pressure system because entire body

• LV pumps oxygenated blood to body, deoxygenated blood returns to RA

Conduction system

SA node (pacemaker) → AV node → Bundle of His → Bundle branches → Purkinje fibers

Cardiac cell action potential

• Depolarization: sodium enters cell for electrical activation

• Plateau: calcium enters the cell to trigger contraction

• Repolarization: potassium exits the cell to reset electrically

Refractory period

There should be no contraction during this time so your heart can relax without being reactivated and fill with blood

• absolute refractory period: cells cannot be re-stimulated

• protects against fatal arrhythmias

Acute coronary syndrome

Sudden reduction of blood flow to heart muscle AKA myocardial ischemia

• STEMI, NSTEMI - ischemia + infarction + troponin elevated

• unstable angina - ischemia + no infarction + no troponin elevated

Angina pectoris

Chest pain

• unstable angina is new, worsening, or unpredictable chest pain not relieved with rest, it IS a medical emergency

• chronic stable is consistent, chronic pain relieved with rest/nitroglycerin

• Prinzmetal’s: coronary artery spasm

• microvascular angina

Unstable angina - risk factors

• arteriosclerosis

• smoking, diabetes, hypercholesterolemia, metabolic syndrome

Pathophysiology of unstable angina

1. Oxygen supply cannot meet oxygen demand of cardiac tissue

2. coronary flow reserve: ability of coronary blood flow to increase when the heart needs more oxygen (with narrowed/dysfunctional coronary arteries, they cannot increase blood flow enough)

• can result in ischemia, that leads to lactic acid formation, contributing to angina

3. Coronary thrombus: blockage from atherosclerotic plaque

4. Prinzmetal’s angina: Coronary artery vasospasm → temporary narrowing → decreased blood flow → ischemia

5. Ischemia with no obstructive coronary artery (INOCA): microvascular angina without obstruction

6. Anemia: less oxygen delivered to myocardium → can result in angina

Signs and symptoms of unstable angina

• crushing sensation on left side of chest

• Levine’s sign: clenched fist over sternum

• pain radiating to shoulder, jaw, down arm

• pain initiated by exertion or stress

• lasts 1-5 minutes

• no change with alterations in position, respiration, or cough

Anginal equivalents - WOMEN

• signs of MI for women differ from classic angina, which is why they are often missed AND treated less aggressively for possible MI than men

• EX: dyspnea, feeling faint, epigastric pain, extreme fatigue

Diagnosis of unstable angina

• blood lipids

• blood pressure

• ECG: ST elevation - not confirmatory

• CRP

• cardiac troponin - confirmatory test for MI because heart muscles release troponin when they die

• chest X-ray to differentiate between cardiac vs. respiratory abnormality

• calcium CT

• cardiac angiogram - gold standard BUT risk of rupturing atherosclerotic plaque

• noninvasive CT angiography - decreased risk of plaque rupture

• graded exercise stress test to determine areas of injury

Treatment of unstable angina

• education, modification of lifestyle risk factors

• nitrates: vasodilators

• aspirin: decrease platelet adherence

• beta blockers: decrease myocardial oxygen demand

• calcium antagonists: arteriole dilation

• ACE inhibitors: decrease BP and resistance

• MONA vs. THROMBINS2

Surgical and endovascular options for unstable angina

Percutaneous transluminal coronary angioplasty (PCTA)

• angioplasty: inflated balloon pushes plaque against arterial wall

• atherectomy: catheter with blade removes plaque

• stent: maintains open vessel, antiplatelets (risk for bleeding)

Coronary artery bypass graft (CABG)

• creates new routes around occlusions

• saphenous vein of leg often used

• x3, x4, x5 bypasses

• traditionally cardiopulmonary heart pump used, but currently uses off pump procedures where heart still pumps during procedure

Chronic stable angina

Recurring episodes of chest pain

• predictable pain relieved by rest and nitroglycerin

• “inactive” atherosclerotic plaque

• surgical treatment NOT an option

Prinzmetal’s angina - characteristics, diagnosis, treatment

• vasospastic angina where coronary artery suddenly spasms, temporarily reducing blood flow

• not associated with typical CAD risk, EXCEPT for smoking, inflammatory states (high CRP levels)

• associated with migraines, Raynaud’s phenomenon

occurs at rest, think: charley’s horse in your arteries

diagnosis: 24 hour cardiac monitoring, coronary angiography, cardiac enzymes

treatment: nitrates, calcium channel blockers to help dilate and relax

Acute myocardial infarction

Prolonged cardiac tissue ischemia

• irreversible damage due to atherosclerotic plaque, thrombus, increased myocardial demand

Factors that determines MI damage

• location: determines which part of heart is damaged (EX: LV damage = decreases pumping ability = heart failure)

• length of time: greater than 30 minutes of ischemia causes irreversible damage

• collateral circulation: alternate blood vessels that provide blood/oxygen to ischemic area (more collateral circulation = less damage)

• zone of injury: surrounds zone of ischemia where there are some recoverable cells

• necrotic cells: release troponin

Reperfusion injury

Too fast reperfusion can be damaging

• AKA myocardial stunning

• Reperfusion injury may be due to oxidized free radicals generated by WBCs

MI signs and symptoms

• SAME AS UNSTABLE ANGINA

• also, sweating, nausea, anxiety, silent MI

• anginal equivalents (women)

ECG diagnosis for MIs

• ECG cannot confirm MI, can show location

  • STEMI: ST elevation MI; all the layers of the heart

  • NSTEMI: non-ST segment elevation MI; subendocardial and NOT completely through heart wall

Blood test diagnosis for MIs

• CPK-MB: cardiac enzyme (creatine kinase)

  • rise within 4 hours of MI, peaks around 12-24 hours, subsides over 3 to 4 days

  • less specific than troponin

• cTnI: cardiac troponin

  • rises 4-8 hours after myocardial injury, remains elevated for several days

  • GOLD STANDARD to diagnose because it shows cardiac tissue death

• hs-cTnI: high sensitivity cardiac troponin assay

  • better at detecting early MIs

  • highly specific for cardiac muscle necrosis

  • GOLD STANDARD to diagnose acute MI

Treatment for MI

SAME AS UNSTABLE ANGINA

• thrombolytic agents: breaks up clots

MI complications

• post-MI dysrhythmias

  • risk greatest after MI

• reentry - cause of dysrhythmias

  • electrically unstable conduction

  • impulses may reactivate already depolarized areas, causing dysrhythmias

• papillary muscle rupture (helps keep AV valves closed during ventricular contraction)

  • if in LV, mitral valve is affected: mitral regurgitation, backup of blood into LA and pulm. pressure increases, dyspnea + crackles

• thromboembolism

  • poorly contracting heart chambers cause stagnant blood, increasing risk for clot formation

• ventricular aneurysm and rupture

• pericarditis

  • occurs 2-3 days post-MI

  • pericardial friction rub, stabbing pain with inspiration

  • may occur as component of Dressler’s syndrome: hypersensitive reaction to tissue necrosis in MI

MI complications - heart failure

• Left sided HF: LV damaged, fluid backs up into pulmonary circulation (lungs) leading to dyspnea, crackles, pulmonary edema, difficulty breathing, hypotension

• Right sided HF: RV damaged, fluid backs up into systemic circulation (body/venous system) leading to jugular vein distention and peripheral edema - fluid accummulation

MI complications - cardiogenic shock

The heart cannot pump enough blood to meet the body’s needs

• acute MI accounts for 81% of patients in cardiogenic shock

Ventricles fail to pump sufficient blood so BP drops, cardiac output drops, and poor perfusion of organs cause organ failure

Infectious endocarditis

• Growth of bacteria (staphylococcus aureus) that damages heart valves

• risk factors:

  • prosthetic valves, pacemakers, intravascular devices, IV drug usage because they introduce potential for bacteria to come in

  • pneumonia, polynephritis (infection of kidneys traveling to heart), dental procedures

• Vegetation can develop on valve and break off and enter bloodstream (septic emboli)

• Native valve endocarditis: Group A beta hemolytic streptococus (GABHS) from strep throat can trigger rheumatic fever which can damage the heart valves and increase risk of rheumatic valve disease

• new or worsening heart murmur is important sign

Diagnosis and treatment of infectious endocarditis

Diagnosis: 3 blood cultures drawn 12 hours apart

• echocardiographic findings

Treatment

• antibiotics: IV 6 weeks or longer, pt at risk for c.diff

• high dose oral and depot (slow release) antibiotics may be viable

• blood cultures repeated daily until clear

• persistent fever may be present despite antibiotic therapy due to paravulvular or extracardiac abscesses

• surgical intervention

Myocarditis

AKA inflammatory cardiomyopathy = inflammation of heart muscle

• mild to lethal disorder

• common cause: viruses (influenza, herpesvirus, hepatitis)

• autoimmune diseases, toxin exposure

• symptoms: fever, myalgia (muscle pain), arthralgia (joint pain), palpitations

• pericardial friction rub and S3 gallop (extra heart sounds) may be present

Myocarditis diagnosis and treatment

Diagnosis: CBC, ESR, CRP

• cTnI may be elevated indicating myocardial damage

• viral antibody titers should be measures

Treatment: reduce myocardial workload and treat underlying etiology

• reduced activity for >6 months

• treatments to support the heart: ACE inhibitors, inotropic agents (changes strength of heart’s contraction)

Pericarditis

Inflammation of pericardium and epicardium

• pericardial effusion: excess fluid in pericardial tissue

• cardiac tamponade: fluid accumulation begins to compress the heart

• acute pericarditis: sudden inflemmation of pericardium; can mimic MI

• Dressler’s syndrome: specific form of pericarditis after MI (immune-mediated reaction)

Pericarditis - presentation, diagnosis, treatment

Presents with chest pain, fever, pericardial friction rub that worsens with deep breathing

• Beck triad: hypotension, visible jugular vein distention, muffled heart sounds

• pulsus paradoxus: decrease in SBP by 10 mm Hg or more with inspiration as LV can’t fill normally

Diagnosis: echocardiogram, cardiac MRI

Treatment: depends on etiology