Disorders of Cardiac Function, Heart Failure, and Circulatory Shock

Serous pericardium

thin membrane with two layers of parietal and visceral

Endocardium

innermost layer; lines the chambers of the heart and covers the heart valves

Myocardium

middle layer; composed of cardiac muscle tissue

Epicardium

outermost layer; visceral layer of the serous pericardium

Right and left coronary arteries

branch of aorta immediately distal to the aortic valve

Left coronary artery divides into

left anterior descending or interventricular artery; left circumflex artery

Right coronary artery divides into:

right marginal artery, posterior interventricular artery

Coronary artery disease

occurs when atherosclerotic plaques build up in the coronary arteries and narrow the arterial lumen and reduce blood flow to the heart muscle

Possible manifestations or complications of CAD

angina attacks, myocardial infarction, cardiac arrhythmias, heart failure, sudden death

Chronic ischemic heart disease variants

stable angina, variant angina, silent myocardial ischemia

Acute coronary syndrome

no ST-segment elevation - unstable angina, non-st-segment elevation AMI

ST-segment elevation - Q-wave AMI

Chronic ischemic heart disease (CIHD)

there is a deficit of oxygen supply to meet myocardial needs

Angina

chest pain that may occur in different patterns - recurrent, intermittent brief episodes of substernal chest pain, triggered by physical or emotional stress

Angina attacks vary in severity and duration but become

more frequent and longer as disease progresses

Stable angina

triggered by physical exertion or emotional stress: pain with exertion when heart’s oxygen demand increases

Variant angina

cyclical spasms in coronary arteries without increased cardiac workload (pain occurs at rest)

Unstable angina

attacks last longer than stable angina and can be less responsive to medication; prolonged pain at rest may precede to acute coronary syndrome

Silent myocardial ischemia

occurs without pain; reduced blood flow and oxygen supply to the heart muscle without noticeable symptoms

Areas of angina

sweating, shortness of breath, nausea, pain in chest, pain infrequently

CIHD screening

aims to identify asymptomatic stages and reduce the risk of complications

Stress test

monitors heart activity and coronary perfusion during exercise

Treatment of angina attack

rest, stop activity, sublingual nitroglycerin - dilates coronary arteries, improves blood flow to myocardium

Acute coronary syndrome

occurs with sudden, severe reduction in blood flow to myocardium due to severe narrowing or complete blockage of a coronary artery

Atherosclerosis with rupture of plaque is most common cause

thrombus can form at the site of a ruptured atherosclerotic plaque and partially or completely block the coronary artery

Manifestations of Acute Coronary Syndrome

• chest pain may occur at rest and may not be relieved by administration of vasodilators

• pain is substernal, crushing radiating

• feeling of pressure, heaviness, burning in chest

• sudden SOB, weakness, fatigue

• nausea, indigestion

Ischemia

inadequate blood (O2) supply alters electrical activity of myocardial cell

Critical part of ECG when the

ventricles are fully depolarized and contracting to eject blood

ECG changes indicate

high probability of MI

ST-segment elevation (STEMI)

likely coronary thrombus occluding artery

Abnormal Q waves

no depolarizing current conducting from necrotic tissue

NSTEMI

lack of ST segment elevation suggests the clot only partly occludes coronary artery

T-wave inversion

repolarization of ventricle altered due to myocardial ischemia or MI

STEMI Treatment

percutaneous coronary intervention (PCI), thrombolytics, anticoagulants

NSTEMI treatment

pharm treatment to reduce myocardial workload, anticoagulants, monitor ECG and serum markers checked, angioplasty if not stable

Percutaneous coronary intervention (PCI)

balloon angioplasty to widen narrowed arteries

stent placement to keep the artery open

Myocardial Infarction

evidence of myocardial necrosis in a clinical setting consistent with acute myocardial ischemia

Time limit

irreversible damage and necrosis may begin within 20-40 minutes of severe coronary artery occlusion

Cardiac markers

substances released into the bloodstream when the heart muscle is damaged

Troponin 1

a preferred marker due to its high sensitivity and specificity, may rise within 3-6 hours after symptom onset

Myoglobin

rises within approximately 2 hours after myocardial injury; is not specific to the heart because it is also found in skeletal muscle

CK-MB (creatine kinase-MB)

increases within 6-8 hours after myocardial injury

Complications of MI

sudden death, cardiogenic shock, cardiac tamponade, thromboembolism, ventricular aneursym

Cardiac tamponade

rupture of necrotic heart tissue with blood accumulation in pericardium

Ventricular aneursym

bulging of a weakened area of the ventricular wall

Cardiac cycle

sequence of events that occurs during one complete contraction and relaxation of the heart

Diastole

relaxation phase

Diastole movements

• ventricles relax and pressure decreases

• mitral and tricuspid valves open, blood flows from atria to ventricles

Systole

contraction phase

Systole movements

• ventricular pressure increases as heart muscle contracts

• mitral and tricuspid valves close, aortic and pulmonic valves open

• blood ejected into aorta and pulmonary artery

Cardiac output

amount of blood pumped by one ventricle in one minute

Cardiac output (CO) =

Heart rate (HR) x Stroke volume (SV)

Stroke volume

amount of blood ejected by one ventricle during each contraction

Stroke volume =

End-diastolic volume (EDV) - End-systolic volume (ESV)

Preload

degree of myocardial stretch before contraction

Increased myocardial stretch leads to an

increased stroke volume

Preload depends on primarily on

end-diastolic volume (EDV) and venous return

Afterload

resistance the ventricles must overcome to eject blood during contraction

Afterload is primarily determined by

arterial pressure and peripheral vascular resistance

Major component of afterload

pressure in the arteries pushing on SL valves

Increased afterload

decreases stroke volume

Ejection fraction (EF)

percentage of blood that is pumped by ventricle with each contraction

Normal - 55-75%; EF below 50% is considered low

Cardiac reserve

ability to increase CO to meet the body’s increased demands during physical activity or stress

Heart failure (HF)

clinical condition in which the heart cannot pump out sufficient blood to meet metabolic needs for oxygen and nutrients

The body activates several compensatory mechanisms to

maintain blood flow to vital organs when the heart’s pumping function declines

When heart cannot maintain pumping capability

cardiac output or stroke volume decreases (EF below 45%) so less blood reaches organs and mild acidosis develops

Backup and congestion develop as

output from ventricle is less than the inflow of blood

Systolic heart failure

decreased contractility; weakness and dilation of ventricle so heart has difficulty contracting and ejecting blood

Diastolic heart failure

decrease filling; stiffness or hypertrophy of ventricles so heart cannot relax and fill with blood

Left-sided heart affected

left ventricle cannot pump blood effectively into the systemic circulation

Right-sided heart affected

right ventricle cannot pump blood effectively into the pulmonary circulation

How left-sided heart failure works

left ventricle weakness and cannot empty, decreased CO, decreased renal blood flow stimulating renin-angiotensin and aldosterone, backup of blood in pulmonary vein, high pressure in pulmonary capillaries leading to pulmonary congestion

How right-sided heart failure works

right ventricle weakens and cannot empty, decreased CO, decreased renal blood flow stimulates renin-angiotensin and aldosterone, backup of blood into circulation, increased venous pressure results in edema in legs, liber, abdominal organs, very high venous pressure causes distended neck vein

Forward effects are

the consequences of reduced blood flow from the heart to the body’s tissues and similar in both left and right

Examples of forward effects

reduced oxygen supply and impaired cellular function

Reduced oxygen supply

cells receive insufficient oxygen to meet their metabolic needs - dyspnea and SOB

Impaired cellular function

reduced oxygen availability decreases cellular energy production - fatigue and weakness

Compensatory mechanisms are activated to

maintain BP and blood flow

Examples of compensatory mechanisms

tachycardia (hypoxia activates SNS), activation of RAAS (due to decreased kidney perfusion)

Backup effects of left-sided heart failure

blood backs up in pulmonary circulation, increases hydrostatic pressure in pulmonary capillaries resulting in pulmonary congestion

Clinical manifestations of left-sided heart failure

SOB, difficulty breathing when lying flat, waking up at night with sudden breathlessness, crackles on lung auscultation, cough sometimes producing pink, frothy sputum

Backup effects of right-sided heart failure

blood backs up into the systemic circulation, increasing hydrostatic pressure in systemic capillaries and forcing fluid into surrounding tissues

Clinical manifestations of right-sided heart failure

dependent edema in the feet & ankles, jugular vein distension, hepatomegaly and splenomegaly, ascites

Congential heart disease

structural defects of the heart that develop during the first eight weeks of embryonic development

Categorizations of congenital heart disease manifestations

valvular defects, septal defects, blood vessel defects, cyanotic, acyanotic

Common clinical manifestations of CHDs

pallor or cyanosis, tachycardia, presence of heart murmur

Valvular heart defects occur when

one or more of the heart’s four valves fail to function properly, disrupting normal blood flow through the heart

Classification of valvular defects

stenosis, valvular incompetence, valve prolapse

Stenosis

narrowed valve will not open all the way and makes it harder for blood to flow through

Stenosis Murmur

blood is forced through the narrowed opening, creating a whooshing sound

Regurgitation

valve does not close completely so valve leaks when it should be closed

Regurgitation murmur

abnormal heart sound caused by blood leaking backward through the valve

The most common cyanotic (R → L shunt) congenital heart condition

tetralogy of fallot

Cyanosis occurs because

shunt bypasses the pulmonary circulation and alters pressure in heart and alters blood flow

Tetralogy - 4 abnormalities

pulmonary stenosis, ventricular septal defect, dextroposition of the aorta, right ventricular hypertrophy

Pulmonary stenosis

narrowing of pulmonary trunk

Ventricular septal defect (VSD)

opening in ventricular septum

Dextroposition of the aorta

aorta is positioned over the VSD

Right ventricular hypertrophy

thickened wall of right ventricle due to increased workload

Pericarditits

inflammation of the pericardium, double layered membrane that surrounds the heart

Pericarditiis is usually secondary to

another condition or injury (open heart surgery, MI, rheumatic fever, SLE, cancer)