Pathophysiology: Chapter Twenty Seven

Coronary circulation

Systemic circulation that delivers oxygen-rich blood to the myocardium through the right and left coronary arteries.

Right coronary artery branches

Right marginal artery and posterior interventricular artery.

Left coronary artery branches

Left anterior descending (interventricular) artery and left circumflex artery.

Coronary artery disease (CAD)

Atherosclerotic plaques narrow coronary artery lumens and reduce blood flow to heart muscle.

Possible complications of CAD

Angina, myocardial infarction, cardiac arrhythmias, heart failure, and sudden death.

Chronic ischemic heart disease (CIHD)

A mismatch in which oxygen supply is insufficient to meet myocardial oxygen needs.

Angina

Recurrent, intermittent episodes of substernal chest pain caused by insufficient oxygen supply to the myocardium.

Stable angina

Chest pain triggered by physical exertion or emotional stress when myocardial oxygen demand increases.

Variant angina

Chest pain caused by cyclical coronary artery spasms, often at rest in the early morning or at night.

Unstable angina

Angina attacks that last longer than stable angina, may respond less to medication, and can precede acute coronary syndrome.

Silent myocardial ischemia

Reduced blood flow and oxygen supply to heart muscle without noticeable pain or other obvious symptoms.

Acute coronary syndrome (ACS)

Sudden, severe reduction in myocardial blood flow from severe coronary narrowing or complete blockage.

Most common cause of ACS in the slides

Atherosclerotic plaque rupture followed by thrombus formation that partially or completely blocks a coronary artery.

ST segment

ECG portion associated with the ventricles being fully depolarized and contracting to eject blood.

STEMI

ST-segment elevation myocardial infarction, often associated with a coronary thrombus occluding an artery.

NSTEMI

Myocardial infarction without ST-segment elevation; the slides associate it with a clot that only partly occludes a coronary artery.

Abnormal Q waves

ECG changes indicating no depolarizing current is conducted from necrotic tissue.

T-wave inversion

Altered ventricular repolarization associated with myocardial ischemia or infarction.

Percutaneous coronary intervention (PCI)

Procedure that can use balloon angioplasty to widen a narrowed artery and a stent to keep it open.

Thrombolytics/fibrinolytics

Medications used to dissolve blood clots.

Anticoagulants

Medications used to prevent clot growth.

Myocardial infarction (MI)

Evidence of myocardial necrosis in a clinical setting consistent with acute myocardial ischemia.

Time to irreversible myocardial injury

Severe coronary artery occlusion may begin causing irreversible damage and necrosis within 20–40 minutes.

Cardiac markers

Substances released into the bloodstream when heart muscle is damaged.

Troponin I

Preferred cardiac marker in the slides because of high sensitivity and specificity; may rise 3–6 hours after symptom onset.

Myoglobin

Marker that may rise about 2 hours after myocardial injury but is not heart-specific because skeletal muscle also contains it.

CK-MB

Creatine kinase-MB; cardiac marker that increases within about 6–8 hours after myocardial injury.

Complications of MI

Sudden death, cardiogenic shock, cardiac tamponade, thromboembolism, and ventricular aneurysm.

Cardiac tamponade

Pressure from fluid or blood around the heart that limits cardiac filling.

Cardiac cycle

Sequence of events during one complete contraction and relaxation of the heart.

Diastole

Ventricular relaxation and decreased pressure; mitral and tricuspid valves open so blood flows from atria into ventricles.

Systole

Ventricular contraction raises pressure; mitral and tricuspid valves close, aortic and pulmonary valves open, and blood is ejected.

Cardiac output (CO)

Amount of blood pumped by one ventricle per minute; CO = heart rate × stroke volume.

Average adult cardiac output

Approximately 5 L/min in a healthy adult, according to the slides.

Stroke volume (SV)

Amount of blood ejected by one ventricle during each contraction.

Stroke volume formula

SV = end-diastolic volume (EDV) − end-systolic volume (ESV).

Average stroke volume

Approximately 70 mL, according to the slides.

Preload

Myocardial stretch before contraction; depends primarily on EDV and venous return.

Effect of increased preload

Increased myocardial stretch can increase stroke volume.

Afterload

Resistance the ventricles must overcome to eject blood; primarily determined by arterial pressure and peripheral vascular resistance.

Effect of increased afterload

Increased afterload decreases stroke volume.

Ejection fraction (EF)

Percentage of ventricular blood pumped out with each contraction.

Normal ejection fraction

55–75% according to the slides; EF below 50% is considered low.

Cardiac reserve

Ability to increase cardiac output to meet increased demands during physical activity or stress.

Heart failure (HF)

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

Systolic heart failure

Weakness and dilation of the ventricle make contraction and blood ejection difficult.

Diastolic heart failure

Ventricular stiffness or hypertrophy prevents adequate relaxation and filling.

Left-sided heart failure

Left ventricle cannot pump blood effectively into systemic circulation; blood backs up into pulmonary circulation.

Right-sided heart failure

Right ventricle cannot pump blood effectively into pulmonary circulation; blood backs up into systemic circulation.

Forward effects of heart failure

Reduced blood flow to tissues causes inadequate oxygen delivery, impaired cellular energy production, dyspnea, fatigue, and weakness.

Compensatory tachycardia in HF

Increased heart rate helps maintain cardiac output when pumping function declines.

RAAS activation in HF

Decreased kidney perfusion activates the renin–angiotensin–aldosterone system, promoting vasoconstriction and sodium/water retention.

Left-sided HF manifestations

Shortness of breath, difficulty breathing lying flat, sudden nighttime breathlessness, lung crackles, cough, and possibly pink frothy sputum.

Orthopnea

Difficulty breathing when lying flat, described in the slides as a manifestation of left-sided HF.

Paroxysmal nocturnal dyspnea

Waking at night with sudden breathlessness, described in the slides as a manifestation of left-sided HF.

Right-sided HF manifestations

Dependent edema of feet/ankles, jugular venous distension, hepatomegaly, splenomegaly, and ascites.

Ascites

Marked abdominal distension caused by fluid accumulation.

Congenital heart disease

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

Categories of congenital heart defects

Valvular defects, septal defects, blood vessel defects, cyanotic defects, and acyanotic defects.

Valvular stenosis

Narrowing of a valve that prevents it from opening fully and makes blood flow through it more difficult.

Valvular regurgitation/incompetence

A valve leaks when it should be closed, allowing blood to flow backward.

Valve prolapse

One or more valve leaflets bulge abnormally backward into the preceding heart chamber.

Heart murmur with stenosis

Whooshing sound created as blood is forced through a narrowed valve opening.

Heart murmur with regurgitation

Abnormal sound caused by blood leaking backward through a valve.

Tetralogy of Fallot

Cyanotic congenital heart condition involving a right-to-left shunt and four structural abnormalities.

Four abnormalities of Tetralogy of Fallot

Pulmonary stenosis, ventricular septal defect, dextroposition of the aorta over the VSD, and right ventricular hypertrophy.

Right-to-left shunt in Tetralogy of Fallot

Blood bypasses pulmonary circulation, so less blood reaches the lungs and deoxygenated blood enters systemic circulation.

Pericarditis

Inflammation of the double-layered pericardium surrounding the heart.

Pericardial effusion

Accumulation of fluid in the pericardial sac due to inflammation.

Signs associated with pericarditis in the slides

Distended neck veins, faint heart sounds, and possible cardiac tamponade.

Chronic pericarditis

Long-term pericardial inflammation causing adhesions that restrict heart movement during systole and diastole and reduce cardiac output.

Rheumatic fever

Acute systemic inflammatory condition caused by an abnormal immune reaction after untreated group A beta-hemolytic Streptococcus infection.

Common age range for rheumatic fever

Most common in children ages 5–15.

Long-term cardiac effect of rheumatic fever

Inflammation and permanent scarring of heart valves; the mitral valve is commonly affected.

Pericarditis, myocarditis, endocarditis

Inflammation of the pericardium, myocardium, and endocardium, respectively.

Antistreptolysin O (ASO) titer

Blood test measuring antibodies against group A Streptococcus.

Infective endocarditis

Infection of the endocardium and heart valves, usually when microorganisms enter the bloodstream and attach to valves.

Predisposing factors for infective endocarditis

Abnormal or damaged valves, bacteremia, and reduced host defenses.

Vegetations in infective endocarditis

Masses of bacteria, platelets, and fibrin that accumulate on heart valves.

Embolic complication of infective endocarditis

Pieces of valve vegetations can break off and travel through the bloodstream.

Acute infective endocarditis

Rapid-onset infection commonly associated with high, spiking fever and chills.

Subacute infective endocarditis

Gradual, insidious infection progressing over days to weeks, with fatigue, anorexia, and shortness of breath.

Cardiomyopathy

Disease of the myocardium associated with mechanical and/or electrical dysfunction and often ventricular hypertrophy or dilation.

Primary cardiomyopathy

Cardiomyopathy classified as genetic, acquired/idiopathic, or mixed.

Secondary cardiomyopathy

Heart muscle disease resulting from an underlying systemic disorder.

Examples of secondary cardiomyopathy causes

Diabetes or thyroid disorders, thiamine deficiency, alcohol, and certain chemotherapy drugs.

Dilated cardiomyopathy (DCM)

Ventricular dilation and enlargement decrease myocardial contractility.

Hypertrophic cardiomyopathy (HCM)

Thickening of ventricular walls and septum reduces ventricular filling; may cause sudden death during exertion.

Shock

Acute circulatory failure to deliver adequate oxygen to tissues, causing cellular dysfunction and potentially organ failure.

Hypovolemic shock

Shock caused by inadequate circulating blood volume.

Cardiogenic shock

Shock in which the heart fails to pump enough blood to maintain adequate circulation.

Distributive shock

Shock in which vasodilation causes abnormal distribution of blood.

Neurogenic shock

Distributive shock caused by CNS, especially spinal cord, damage that removes sympathetic vascular tone and causes vasodilation.

Septic shock

Distributive shock caused by severe systemic infection, with vasodilation, capillary leakage, and circulatory dysfunction.

Anaphylactic shock

Distributive shock caused by a severe type I allergic reaction, leading to vasodilation and increased capillary permeability.

Compensation in shock: SNS

Epinephrine and norepinephrine increase heart rate and cause systemic vasoconstriction.

Compensation in shock: RAAS

Renin activation leads to angiotensin II vasoconstriction and aldosterone-mediated sodium and water retention.

Compensation in shock: ADH

Increased antidiuretic hormone helps retain water and maintain blood volume.

Lactic acid in shock

Reduced tissue perfusion promotes anaerobic metabolism, which produces lactic acid.

Major complications of shock

Acute renal failure, ARDS (shock lung), hepatic failure, paralytic ileus, GI ulcers, infection/septicemia, and DIC.