chapter 27: disorders of cardiac function, heart failure, and circulatory shock

heart is enclosed within the:

pericardium!

serous pericardium

• thin membrane with 2 layers: parietal and visceral

• pericardial cavity is potential space btwn parietal and visceral layers of serous pericardium

heart wall consists of 3 layers:

1. endocardium

2. myocardium

3. epicardium

endocardium

• innermost layer

• lines chambers of heart and covers heart valves

myocardium

• middle layer

• composed of cardiac muscle tissue

epicardium

• outermost layer

• also called visceral layer of serous pericardium

right and left coronary arteries branch of:

• aorta immediately distal to aortic valve

• part of systemic circulation to deliver oxygen-rich blood to myocardium

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 (CAD)

• aka coronary heart disease

• occurs when atherosclerotic plaques build up in coronary arteries, narrowing arterial lumen and reducing blood flow to heart muscle

• CAD remains silent for many years until blood flow becomes significantly reduced

possible manifestations or complications of CAD

• angina attascks

• myocardial infarction

• cardiac arrhythmias

• heart failure

• sudden death

chronic ischemic heart disease (CIHD)

• occur when deficit ox oxygen supply to meet myocardial needs

• classic symptom: 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

CIHD can be classified into 4 main types:

• stable angina

• variant angina

• unstable angina

• silent myocardial ischemia

stable angina

• often called classic or exertional

• triggered by physical exertion when heart’s O2 demand increases

variant angina

• vasospastic (prinzmetal)

• cyclical spasms in coronary arteries without increased cardiac workload: pain occurs at rest (early morning or night)

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 (angina/type of CIHD)

• occurs without pain

• reduced blood flow and oxygen supply to heart muscle without noticeable symptoms

areas of angina

CIHD management screening:

• aims to identify asymptomatic stages + reduce 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 w/ sudden severe reduction in blood flow to myocardium due to severe narrowing or complete blockage of coronary artery

• severe or prolonged lack of blood flow can cause perm dmg to heart muscle

in acute coronary syndrome, atherosclerosis w/ ruputure of plaque is the most:

• common cause of ACS

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

• size and dmg of obstruction determine dmg

manifestations of acute coronary syndrome:

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

• pain described as substernal, crushing, radiating

• feeling of pressure, heaviness, or burning in chest

• sudden SOB, weakness, fatigue

• nausea, indigestion

acute coronary syndrome ECG ischemia:

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

acute coronary syndrome ECG

• assess ST segment

• critical part of ECG when ventricles fully depolarized and contracting to eject blood

ECG changes that indicate high probability of MI:

• ST-segment elevation (STEMI): likely coronary sthrombus occluding artery

• abnormal Q waves: no depolarizing current conducting from necrotic tissue

ECG changes that indicate intermediate or low probability of MI:

• NSTEMI: lack of ST segment elevation suggests 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)

  • balloon angioplasty to widen narrowed arteries

  • stent placement to keep the artery open

• thrombolytics: dissolve blood clots

• anticoagulants: prevent clot growth

NSTEMI treatment:

• pharm treatment to reduce myocardial workload - beta blockers

• anticoagulants - heparin

• monitor ECG and serum markers checked

• angioplasty if not stable

myocardial infarction

• evidence of myocardial necrosis in clinical setting consistent w/ acute myocardia ischemia

• time limit: irrev dmg + necrosis may begin within 20-49 mins of severe coronary artery occlusion

• cardiac markers: blood lvls of cardiac troponin rise

cardiac markers + types:

• substances released into bloodstream when heart muscle is dmgd

• troponin I, myoglobin, and CK-MB (creatine kinase-MB)

troponin I (cardiac marker)

preferred marker due to its high sensitivity and specificity, may rise within 3-6 hrs after symptoms onset

myoglobin (cardiac marker)

• rise within approx 2 hrs after myocardial injury

• not specific to heart since also found in skeletal muscle

CK-MB (creatine kinase-MB) (cardiac marker)

• increases within 6-8 hrs after myocardial injury

complications of MI:

• sudden death

• cardiogenic shock

• cardiac tamponade: rupture of necrotic heart tissue w/ blood accumulation in percardium

• thromboembolism

• ventricular aneurysm: bulging of weakened area of ventricular wall

cardiac cycle

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

• diastole and systole

diastole (cardiac cycle)

• relaxation phase

• ventricles relax and their pressure decreases

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

systole (cardiac cycle)

• contraction phase

• ventricular pressure increases as heart muscle contracts

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

• blood is ejected into aorta and pulmonary artery

cardiac output (CO)

• amount of blood pumped by one ventricle in one heart

• CO = heart rate x stroke volume

• avg CO ~ 5 L/min in healthy adult

stroke volume (SV)

• amnt of blood ejected by one ventricle during each contraction

• SV calculated by subtracting volume of blood remaining after contraction (ESV) from volume of blood before contraction (EDV)

• stroke volume = end-diastolic volume - end-systolic volume

• avg SV ~ 70 mL

preload

• degree of myocardial stretch before contraction

• increased myocardial stretch leads to increased stroke volume

• preloasd depends primarily on end-diastolic volume (EDV) and venous return

afterload

• resistance ventricles must overcome to eject blood during contraction

• primarily determined by arterial pressure + peripheral vascular resistance

• pressure in arteries pushing on SL valves is major component of afterload

• increased afterload decreases stroke volume (SV)

ejection fraction (EF)

• percentage of blood pumpedby ventricle w/ each contraction

• norm EF: 55-75%

• EF beloe 50% is considered low

cardiac reserve

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

heart failure (HF)

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

• HF usually complication of another cardiopulmonary condition

• body activates several compensatory mechanisms to maintain blood flow to vital organs when heart’s pumping function declines

  • some of them often aggravate condition

when heart cannot maintain pumping capability:

• cardiac output or stroke volume decreases (EF) below 45%

• less blood reaches various organs, cell function and metabolism decreased

• mild acidosis develops

backup and congestion develop as:

• output from ventricle is less than inflow of blood

• congestion in venous circulation draining into affected side of heart

heart failure can be classified accord to:

1. functional problem: systolic and diastolic

2. side of heart affected: left and right sided

functional problem (HF)

• systolic: decreased contractility

  • weakness and dilation of ventricle: heart has difficulty contracting and ejecting blood

• diastolic: decreased filling

  • stiffness or hypertrophy of ventricle: heart cannot relax + fill w/ blood

side of heart affected

• left sided: left ventricle cannot pump blood effectively into systemic circulation

• right sided: right ventricle cannot pump blood effectively into pulmonary circulation

forward effects

• consequences of reduced blood flow from heart to body’s tissues, similar in both left and right sided heart failure

• reduced oxygen supply: cells receive insufficient oxygen to meet metabolic needsL 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

• tachycardia - hypoxia activates SNS

• activation of RAAS - due to decreased kidney perfusion

manifestations of HF - back up effects of left sided HF

• blood backs up into pulmonary circulation, increasing hydrostatic pressure in pulmonary capillaries resulting in pulmonary congestion

• clinical manifestations include:

  • SOB - dyspnea

  • difficulty breathing when lying flat - orthopnea

  • waking up at night w/ sudden breathlessness - paroxysmal nocturnal dyspnea

  • crackles heard on lung auscultation

  • cough, sometimes producing pink, frothy sputum in severe pulmonary edema

manifestations of HF - back up effects of right sided HF

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

• clinical manifestations include:

  • dependent edema in feet and ankles

  • jugular venous distension: veins in neck to become enlarged

  • hepatomegaly and splenomegaly

  • ascites: markely abdominal distention due to fluid

congenital heart diseases

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

• categorized based on structural abnornality + manifestations

  • valvular defects: abnormality in valves

  • septal defects: defect in septum

  • bv defects: abnormality in large arteries

  • cyanotic: blue tint

  • acyanotic: absence of blue-ish tint

CHD manifestations based on severity of defect:

• mild defects may be asymptomatic

• large defects noticed after birth

common manifestations CHD:

• pallor or cyanosis: pale of bluish skin

• tachycardia: occurs w/ very rapid sleeping pulse and frequent pulse deficit

• presence of heart murmur: abnormal heart sound

• if untreated, child may dev HF

valvular heart defects (VHD) occur when one more:

• heart’s four valves fail to function properly, disrupting norm blood flow through heart

• common affected valves: aortic and pulmonary

• classification of valvular defects:

  • stenosis - narrowing

  • valvular incompetence - regurgitation

  • valve prolapse - floppy valve

    • one or more valve leaflets bulge abnormally backward into preceding heart chamber

stenosis (VHD)

• narrowed valve not open all way up

  • harder for blood to flow through

• murmur: blood forced through narrowed opening, creating whooshing sound

regurgitation (VHD)

• valve will not close completely

  • valve leaks when it should be closed

• murmur: abnorm heart sounds caused by blood leaking backward through valve

tetragoly of fallot

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

• cyanosis occurs because shunt bypasses pulmonary circulation

  • alters pressures in heart and alters blood flow

tetralogy includes four abnormalities:

• 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.

pericarditis

• inflammation of pericardium, double layered membrane that surrounds heart

• pericarditis usually secondary to another condition or injury (open heart surgery, MI, rheumatic fever, SLE, cancer)

inflammation that causes fluid to accumulate in pericardial sac is called what?

pericardial effusion!

signs & symptoms of pericarditis

• distended neck veins

• faint heart sounds: fluid surrounding heart can muffle sounds heard through stethoscope

• cardiac tamponade occurs when pressure around heart limits ability to fill w/ blood

chronic pericarditis

• long-term inflammation of pericardium results in formation of adhesions btwn pericardial cavity

• these adhesions restrict heart’s movmnt during diastole and systole, reducing cardiac output

• symptoms result from systemic venous congestion and decreased cardiac output

  • manifestations include: SOB, fatigue, peripheral edema, elevated jugular venous pressure, pleural effusion

rheumatic fever

• acute systemic inflammatory condition result from abnormal immune reaction after untreated infection (group A B-hemolytic streptococcus)

• usually follows strep throat or another group A strep infection

• most common in children ages 5-15

long term effects of rheumatic fever

• rheumatic fever can cause inflammation + permanent scarring of heart valves

• mitral valve is commonly affected

• leading cause of adult mitral valve replacement in US

during acute stage of RA, heart may become

inflamed!

for rheumatic fever’s acute stage, inflammation can affect all 3 layers of heart, which are:

• pericarditis: inflam of pericardium (membrane surrounding heart)

• myocarditis: inflam of myocardium (heart muscle)

• endocarditis: inflam of endocardium (inner lining of heart, which may dmg heart valves)

other areas affected by inflammation from rheumatic fever

• large joints: arthritis, causing joint paint, swelling, tenderness

• skin: vasculitis, associated w/ erythema marginatum (skin rash)

signs & symptoms of rheumatic fever:

• low-grade fever, malaise

• leukocytosis

• tachycardia

• heart murmurs

• erythema marginatum

diagnostic tests of rheumatic fever

• antistreptolysin O (ASO) titer: blood test that measures antibodies against group A streptococcus

• heart function test

infective endocarditis

• infection of endocardium (inner lining of heart and heart valves)

• usually caused by microorganisms, such as bacteria entering bloodstream and attaching to heart valves

predisposing factors for infective endocarditis:

• presence of abnormal valves in heart: dmgd valves make it easier for microorganisms to attach and grow

• bacteremia: bacteria in bloodstream

• reduced host defenses

infective endocarditis - abnormal or prosthetic heart valves:

provide an easy surface for bacteria to attach

infective endocarditis - bacteria, platelets, and fibrin accumulate on:

valves forming masses called vegetations

infective endocarditis - complication

pieces of vegetations may break off and travel through bloodstream - thromboembolism

two common types of infective endocarditis

• acute endocarditis

• subacute endocarditis

acute endocarditis

• rapidly developing, severe, and potentially life-threatening infection of the inner lining of the heart chambers and valves (the endocardium)

• common symptoms: high spiking fever, and chills

subacute endocarditis

• has gradual insidious onset and progresses slowly (over days to weeks)

• common symptoms: increasing fatigue, loss of appetite (anorexia), and SOB

cardiomyopathies

• heterogeneous group of diseases of myocardium associated w/ mechanical and/or electrical dysfunction

• usually (but not invariably) exhibit inappropriate ventricular hypertrophy or dilation and that are due to variety of causes that frequently are genetic

cardiomyopathies either are confined to heart or:

part of generalized systemic disorders, often leading to cardiovascular death or progressive heart failure-related disability

cardiomyopathy classified into 2 main types:

• primary CMP

• secondary CMP

primary cardiomyopathy

• affects heart muscle without any underlying cause

• common types of primary CMP;

  • genetic: caused by inherited gene mutations

  • acquired: idiopathic - exact cause unknown

  • mixed: has both genetic and acquired causes

secondary cardiomyopathy

• heart muscle is affected as a result of underlying systemic disease

• causes and examples of secondary CMP:

  • metabolic disorders: diabetes mellitus or thyroid disorders

  • nutritional deficiencies: thiamine deficiency

  • toxins: alcohol or certain chemotherapy drugs

cardiomyopathy classified into 2 main types based on type of cardiac dysfunction:

• dilated cardiomyopathy (DCM)

• hypertrophic cardiomyopathy (HCM)

dilated cardiomyopathy (DCM):

• ventricular dilation and enlargement lead to decreased myocardial contractility

• systolic function

hypertrophic cardiomyopathy (HCM):

• ventricular hypertrophy (thickening of ventricular walls and septum) causes reduced ventricular filling

• diastolic function

• HCM may lead to sudden death during exertion due to mitral valve regurgitation and atrial thrombus formation

shock

• acute failure of circulatory system to deliver adequate oxygen to body tissues, resulting in cellular dysfunction and, if untreated, organ failure

• classified into 3 main types

  • hypovolemic

  • cardiogenic

  • distributive

hypovolemic (shock)

loss of circulating blood volume

cardiogenic (shock)

heart fails to pump enough blood to maintain adequate circulation

distributive (shock)

vasodilation causes abnormal distribution of blood

distributive shock incldue4s three subtypes:

• neurogenic shock

• septic shock

• anaphylactic shock

neurogenic shock

caused dmg to CNS, especially spinal cord, leading to loss of sympathetic vascular tone and vasodilation

septic shock

caused by severe, systemic infection, leading to vasodilation, capillary leakage, and circulatory dysfunction

anaphylactic shock

caused by severe allergic reaction (type I) that releases inflammatory mediators, leading to vasodilation and increased permeability

SNS and adrenal medulla stimulation releases:

• epinephrine and norepinephrine

• increased heart rate

• systemic vasoconstriction

increased renin secretion:

• happens when the kidneys detect low blood pressure, low blood volume, or low sodium levels

• angiotensin II causes vasoconstriction

• aldosterone increases sodium and water retention