24. Cardiac Disease and Shock Flashcards
volume of blood ejected by ventricle w/ each beat
stroke volume (SV)
volume in LV just before ejection
preload (aka EDV)
fraction of EDV ejected in each stroke volume (how much blood left the ventricle w/ each contraction)
ejection fraction
How to calculate EF
EF% = SV/EDV (usually about 55%)
total volume of blood ejected by ventricle per minute
cardiac output
How to calculate CO
CO = SV x HR (usually about 5 L/min)
Pressure required to eject blood (open aortic valve)
afterload
resistance to blood flow in systemic circulation
peripheral vascular resistance (PVR)
increased PVR increases what?
afterload -> more pressure to push blood out of heart if pressure is higher is system
Increased preload is a result of what?
- hypervolemia - renal failure - regurgitation of cardiac valves
Increased afterload is a result of what?
- hypertension - vasoconstriction
Explain how increased preload can lead to decreased SV and heart failure
- increased preload -> stretching of myocardium -> decreased contractility -> decreased SV + increased ventricular end-diastolic pressure -> pressure backs into pulmonary and venous systems (pulmonary and peripheral edema)
lipoprotein responsable for delivery of cholesterol to the tissues
LDL
lipoprotein responsible for transport of excess cholesterol from the tissues to the liver
HDL
Optimal levels for total cholesterol, LDL, and HDL
- total cholesterol: <200 mg/dL - LDL: <100 mg/dL - HDL: >60 mg/dL
condition characterized by thickening and hardening of the vessel wall
arteriosclerosis
form of arteriosclerosis that is caused by accumulation of lipid-laden macrophages within the arterial wall which leads to the formation of a lesion called a plaque
atherosclerosis
6 possible causes of endothelial injury
- smoking - HTN - DM - increased LDL - decreased HDL - autoimmunity
Explain the pathophysiology of atherosclerosis
- injury to endothelial cells in artery wall -> inflammation - inflammatory process summons macrophages and produces oxygen free radicals - LDL becomes oxidized (causes additional recruitment) - macrophages engulf oxidized LDL -> foam cells - accumulation of foam cells = fatty streak - fatty streak + collagen from injured vessel = fibrous plaque - plaques may occlude blood flow or rupture (rupture initiates clotting and thrombus formation -> ischemia -> infarction)
plaques that have ruptured are called what?
complicated plaques
What usually causes CAD?
atherosclerosis (plaque formation)
develops if flow or O2 content of coronary blood is insufficient to meet metabolic demands of myocardial cells
myocardial ischemia
plaques that are prone to rupture
unstable plaques
Explain how coronary occlusion leads to myocardial infarction
- myocardial cells become ischemic in 10 seconds of occlusion - cells deprived of glucose needed for aerobic metabolism -> switch to anaerobic (lactic acid accumulation) - heart cells lose ability to contract -> CO decreases
How long can myocardial cells go without O2 before myocardial infarction
about 20 minutes
angina caused by gradual luminal narrowing and hardening of arterial walls; consistent type of pain
stable angina pectoris
clinical manifestation of stable angina pectoris
- transient substernal chest pain (may be mistaken for indigestion) - pallor, diaphoresis, and dyspnea (may all be associated w/ pain)
common symptoms of stable angina pectoris seen in women
- atypical chest pain - palpitations - sense of unease - severe fatigue
What relieves stable angina pectoris?
rest and nitrates
chest pain attributable to to transient ischemia of myocardium that occurs unpredictably and often at rest; caused by vasospasm of one or more major coronary arteries with or without atherosclerosis
prinzmetal angina (varient angina)
myocardial ischemia that may not cause detectable symptoms
silent ischemia
2 things linked to silent ischemia
DM and chronic stress
angina that is increasing in severity or frequency, new-onset, or at rest; result of reversible myocardial ischemia and is a sign of impending infarction
unstable angina
results when there is prolonged ischemia causing irreversible damage to heart muscle
myocardial infarction (MI)
EKG changes during unstable angina
ST depression and T wave inversion
procedure whereby stenotic (narrowed) coronary vessels are dilated w/ a catheter
percutaneous coronary intervention (PCI)
persistent coronary occlusion leads to infarction of the myocardium closest to the endocardium
non-STEMI
EKG signs of non-STEMI
ST depression and T wave inversion without Q waves
continued coronary occlusion that leads to transmural infarction extending from endocardium to pericardium
STEMI
EKG signs of STEMI
marked elevations of ST segments
explain how acute mental stress can lead to MI or sudden cardiac death
- stress -> ANS activity -> increased HR, BP and coronary constriction - atherosclerosis or poor LV function -> increased demand and decreased supply - leads to ischemia, plaque rupture, and thrombosis (from platelet activity) - may also cause electrical instability -> VFib/Vtach
temporary loss of contractile function that persists for hours to days after perfusion has been restored
myocardial stunning
describes tissue that is persistently ischemic and undergoes metabolic adaptation to prolong myocyte survival until perfusion is restored
hibernating myocardium
classic signs of myocardial infarction
- heavy/crushing chest pain - pain may radiate to neck, jaw, back, shoulder, or left arm - N/V - diaphoresis
4 areas of damage caused by HTN
- retina - renal disease - CAD/CHF - neurologic disease (stroke, dementia, encephalopathy)
HTN caused by an underlying disorder (ex. renal disease)
secondary HTN
What factors lead to HTN
- genetics + environment - obesity, adipokines, insulin resistance - dysfunction of SNS, RAAS, and ANP/BNP - inflammation
How do the factors leading to HTN cause damage
- vasoconstriction -> increased PVR - renal salt and H2O retention -> increased blood volume - increased PVR + increased volume -> sustained HTN and vascular remodeling
rapidly progressive HTN in which diastolic pressure is usually greater than 140 mmHg
hypertensive crisis (malignant HTN)
name 3 acute coronary syndromes (ACS)
- unstable angina - non-STEMI - STEMI
when the heart is unable to generate adequate CO -> decreased perfusion of tissues or increased diastolic of LV filling pressure
heart failure
how is left heart failure/congestive heart failure categorized
whether there is reduced ejection fraction or persevered ejection fraction
ejection fraction <40% and an inability of the heart to generate adequate CO to perfuse tissues
heart failure w/ reduced ejection fraction (HFrEF) or systolic HF
3 major determinants of stroke volume
- contractility - preload - afterload
Explain how increased PVR can lead to heart failure
- increased PVR -> increased afterload (increased resistance to ventricular ejection) - increased workload in LV - increased RAAS and SNS - hypertrophy - increased myocyte demand for O2 (reactive ischemia) - ventricular remodeling - decreased contractility (decreased CO and perfusion of tissues)
RAAS and SNS release what neurohormones that play a role in ventricular remodeling?
- angiotensin II (aldosterone and vasoconstriction) - aldosterone (retain Na and H2O) - catecholamines (increased HR and BP) - cytokines (inflammation)
symptoms of left heart failure (CHF)
- paroxysmal nocturnal dyspnea - cough (w/ frothy/pink-tinged sputum) - orthopnea - exertion dyspnea - fatigue - decreased urine output - edema
Exam findings of left heart failure (CHF)
- cyanosis - inspiratory crackles - pleural effusions - HTN or hypotension
What serum level will be elevated in left heart failure (CHF)
serum B-type natriuretic peptide (BNP)
pulmonary congestion despite a normal stroke volume and CO; results from increased LVEDP which reflects back into pulmonary and venous system
heart failure w/ preserved ejection fraction (HFpEF) or diastolic heart failure
inability of the RV to provide adequate blood flow into pulmonary circulation; usually due to preceding left heart failure
right heart failure
clinical manifestations of right heart failure
- fatigue - distended jugular veins - ascities - edema - anorexia and GI distress
inability of the heart to adequately supply body w/ blood-borne nutrients despite adequate blood volume and normal or elevated myocardial contractility
high-output failure
condition of excess fluid in the lungs
pulmonary edema
valve orfice is constricted and narrowed so blood cannot flow forward and the workload of the cardiac chamber proximal to the diseased valve increases
valvular stenosis
valve leaflets (cusps) fail to shut completely -> allow blood to flow backwards into previous chamber (increases volume heart must pump and workload)
valvular regurgitation (insufficiency/incompetence)
most common valvular abnormality
aortic stenosis
3 causes of aortic stenosis
- congenital bicuspid valve degeneration - changes w/ aging - rheumatic heart disease
cardiovascular and pulmonary outcomes of aortic stenosis
- LV hypertrophy -> left heart failure - pulmonary edema
impairs blood flow of blood from LA to LV; leads to LA hypertrophy and right heart failure
mitral stenosis
most common form of rheumatic heart disease
mitral stenosis
results from inability of aortic valve leaflets to close properly during diastole; leads to LV hypertrophy and left heart failure
aortic regurgitation
causes of aortic regurgitation
- infective endocarditis - connective tissues diseases (Marfan syndrome) - dilation of aortic root from HTN or aging
permits back flow of blood into LA from LV; leads to LA hypertrophy and left heart failure
mitral regurgitation
causes of mitral regurgitation
- MVP - rheumatic heart disease - infective endocarditis - MI - connective tissues diseases (Marfan syndrome) - dilated cardiomyopathy
permits back flow from RV to RA; usually due to functional problem with the valve (congenital)
tricuspid regurgitation
valvular abnormalities that cause systolic murmur
- aortic stenosis - mitral regurgitation (heard throughout) - tricuspid regurgitation (heard throughout)
valvular abnormalities that cause diastolic murmur
- mitral stenosis - aortic regurgitation
when one or both cusps of mitral valve billow upward into LA during systole
mitral valve prolapse (MVP)
painful, red, raised lesions found on the hands and feet. They are associated with a number of conditions, including infective endocarditis, and are caused by immune complex deposition
Osler’s nodes
non-tender, small erythematous or haemorrhagic macular or nodular lesions on the palms or soles only a few millimeters in diameter that are indicative of infective endocarditis
Janeway lesions
systemic, inflammatory disease caused by delayed exaggerated response to infection by group A B-hemolytic streptococcus (pharyngeal infection only)
rheumatic fever
antibodies directed against M proteins of streptococci cross-react w/ tissues of heart
rheumatic heart disease (RHD)
symptoms of rheumatic fever
- fever - lymphadenopathy - N/V and ABD pain - arthralgia - epistaxis - tachycardia
general term used to describe infection and inflammation of the endocardium (especially valves)
infective endocarditis
Risk factors for introduction of bacteria into endocardium
- dental, GU, or cardiac procedures - skin, wound, lung, or GU infections - indwelling catheters - injection drug use
signs and symptoms of infective endocarditis once vegetation forms
- fever, night sweats, malaise, weight loss - heart murmurs and failure - embolization of vegetation -> abscesses, petechiae, splinter hemorrhages, Osler nodules, and Janeway lesions, right-side emboli = PE; left-side emboli = stroke
acute inflammation and rubbing together of layers of the pericardium
acute pericarditis
symptoms of acute pericarditis
sharp stabbing chest pain behind the sternum in left chest
constriction of the pericardium which results in decreased pump power
chronic/constrictive pericarditis
compression of the heart due to fluid accumulation within the pericardium
pericardial effusion
cardiovascular system fails to perfuse tissues adequately -> widespread impairment of cellular metabolism
shock
What is missing from cells in all types of shock? What is a common finding in all types of shock?
- oxygen (either not receiving or not able to use it) - decreased CO
Describe the effects of impaired O2 delivery and use in shock
- no O2 -> anaerobic metabolism -> decrease ATP and increase lactic acid - increased lactic acid -> metabolic acidosis - decrease ATP -> decrease Na/K pump -> increased intracellular volume (cellular edema) -> decreased circulatory volume - cellular edema -> lysosomal enzymes -> inflammation and activation of clotting cascade
Describe the effects of impaired glucose delivery and use in shock
- increased serum cortisol, thyroid hormone, and catecholamines -> increased lipolysis, gluconeogenesis, and glycogenolysis - lypolysis = increased serum triglycerides - glycogenolysis = decreased energy stores - gluconeogenesis = proteins used for fuel, decrease albumin and increased urea and ammonia formation - muscle wasting and build up of metabolic products
How does the body compensate for shock
- decrease CO and tissue perfusion -> SNS activation - increased BP, HR, and contractility - RAAS activation (retain Na and H2O to increase preload) - vasoconstriction and activation of ADH -> increase preload - increased volume and CO -> restoration of perfusion
4 types of shock
- hypovolemic - cardiogenic - distributive - obstructive
decreased CO and evidence tissue hypoxia in the presence of adequate intravascular volume (heart cannot contract effectively; fluid volume not affected)
cardiogenic shock
causes of cariogenic shock
direct pump failure - MI, cardiac arrest - ventricular dysrhythmia
signs and symptoms of cariogenic shock
- confusion - tachycardia - hypotension - tachypnea - venous and pulmonary edema - oliguria (urine output < 30mL/hour) - dusky skin color; skin cold and clammy
caused by loss of whole blood (hemorrhage), plasma (burns), or interstitial fluid (diaphoresis, DM, DI, emesis, diarrhea, or diuresis) in large amounts
hypovolemic shock
signs and symptoms of hypovolemic shock
- hypotension - tachypnea - tachycardia (weak pulse) - hypoxia - decreased/absent urine - thirst, agitation, anxiety, confusion - skeletal muscle weakness - cold, clammy, cyanotic skin
shock due to decreased vascular volume or tone -> vasodilation w/ pooling causes decrease preload, SV, and CO
distributive shock
3 types of distributive shock
- neurogenic shock - anaphylactic shock - septic shock
result of widespread and massive vasodilation due to parasympathetic overstimulation and sympathetic understimulation
neurogenic/vasogenic shock
results from widespread hypersensitivity reaction known as anaphylaxis
anaphylactic shock
signs and symptoms of anaphylactic shock
- vasodilation and increase capillary permeability (due to histamine) -> hypovolemia - decreased contractility and dysrhythmia - bronchial edema and pulmonary obstruction - widespread hypoxia
toxins and endotoxins related into blood cause systemic inflammatory response syndrome (SIRS); metabolism becomes anaerobic due to decreased MAP, clot formation in capillaries, and poor cellular uptake of O2
septic shock
signs of sepsis
- bacteremia + SIRS - SIRS: fever, tachycardia, tachypnea, leukocytosis
septic shock is related to what clotting abnormality
DIC
shock due to fluid shift from blood to interstitial space
capillary leak
shock due to indirect pump failure (cardiac tamponade, or PE); cardiac function decreases by non-cardiac factors (total body fluid not affected)
obstructive shock
signs of cardiac tamponade
- JVD - paradoxical pulse - decrease CO - muffled heart sounds
signs of PE
- sudden onset dyspnea and pleuritic chest pain - apprehension/restlessness/ feeling of impending doom - cough/hemoptysis - tachypnea and decreased O2 - diaphoresis and low grade fever
progressive dysfunction of 2 or more organ systems resulting from an uncontrolled inflammatory response to severe illness or injury
multiple organ dysfunction syndrome (MODS)
most common cause of MODS
septic shock
Explain pathogenesis of MODS
- injury/sepsis/trauma -> neuroendocrine response and release of inflammatory mediators - activation of complement, coagulation, and kinin systems (massive systemic inflammatory response) - hypermetabolism - vasodilation and selective vasoconstriction -> maldistribution of blood flow -> hypoperfusion and decreased CO - hypermetabolism and hypo perfusion -> increased O2 demand -> tissue hypoxia/metabolic failure -> acidosis - organ dysfunction
what is induced by extremely severe tissue ischemia or by a pathogen
cytokine storm
describe 4 parts of cytokine storm
- endothelium activated (vasodilates and express adhesion molecules) - monocytes activated (release cytokines) - WBC obstructed capillaries - DIC
autoimmune condition characterized by formation of thrombi filled w/ inflammatory and immune cells; strongly associated w/ smoking
Buergers disease
characterized by attacks of vasospasm in the small arteries and arterioles of the fingers
Raynaud phenomenon
triggers of attacks in Raynaud phenomenon
- cold temperatures - emotional stress - smoking (vasoconstriction)
atherosclerotic disease that perfuses the limbs (especially LEs)
peripheral vascular disease (PVD)
pain w/ ambulation due to gradually increasing obstruction of arterial blood flow to the legs by atherosclerosis in the iliofemoral vessels; seen in arterial PVD
intermittent claudication
3 factors that promote venous thrombosis (triad of Virchow)
- venous stasis (immobility, age, CHF) - venous endothelial damage (trauma, IV meds) - hypercoagulable states (inherited disorders, pregnancy, malignancy, OCP, or HRT)
inadequate venous return over a long period
chronic venous insufficiency (CVI)
A wound on the leg or ankle caused by abnormal or damaged veins; copious serous exudates, brown/tawny skin color
venous stasis ulcer
due to a blood clot just below the surface of the skin
superficial venous phlebitis
vein in which blood has pooled, producing distended, tortuous and palpable vessels; typically involve saphenous veins
varicose vein
test specific for myocardial muscle damage
troponin
sudden onset of thrombus or embolus preventing blood flow distal to the clot
acute arterial occlusion
6 Ps of acute arterial occlusion
- Pain - Paresthesias - Paralysis - Pallor - Pulselessness - Perishingly cold/Poikilothermia
caused by hypercoagulability, injury to a vein, and venous stasis
deep vein thrombosis (DVT)
