Pathophysiology II Exam 4 - CARDIO pt. 2

progression of arterial diseases

coronary artery disease -> myocardial ischemia -> acute coronary syndromes

coronary artery disease

any vascular disorder that narrows or occludes the coronary arteries

coronary artery disease can result in

an imbalance between coronary supply of blood and myocardial demand for oxygen and nutrients causing ischemia or irreversible infarction

most common cause of coronary artery disease

atherosclerosis

non-modifiable risk factors for coronary artery disease

- advanced age

- family history

- male gender or being a woman after menopause

modifiable risk factors for coronary artery disease

- dyslipidemia

- hypertension results in endothelial injury and increase in myocardial demand

- cigarette smoking results in vasoconstriction and an increase in LDL/decrease in HDL

- diabetes and insulin resistance results in endothelial damage and thickening of the vessel wall

- obesity and/or sedentary lifestyle

- atherogenic diet

metabolic syndrome is characterized by

obesity, dyslipidemia, and hypertension

dyslipidemia

abnormal concentrations of serum lipoproteins that has a strong association with coronary artery disease

patho of dyslipidemia

- dietary fat packaged into chylomicrons for absorption in the small intestine

- chylomicrons function by transporting exogenous lipid from the intestine to the liver and the peripheral cells

- primarily contains triglycerides that may be removed and either stored by adipose tissue or used by muscle as an energy source

- remnant contains cholesterol, which is then taken up by the liver

increased LDL as an indicator of coronary risk

plays a role in endothelial injury, inflammation, and immune responses that are important in atherogenesis

decreased HDL as an indicator of coronary risk

responsible for "reverse cholesterol transport," which returns excess cholesterol from the tissues to the liver

other indicators of coronary risk

- elevated serum VLDL (triglycerides)

- increased lipoprotein (a)

non-traditional risk factors for coronary artery disease

- markers of inflammation, ischemia, and thrombosis (C-reactive protein)

- chronic kidney disease

- adipokines and other obesity complications

- medications

- microbiome

- air pollution and ionizing radiation

- coronary artery calcification, carotid wall thickness

transient myocardial ischemia

develops if the supply of coronary blood cannot meet the demand of the myocardium for oxygen and nutrients, but perfusion is restored before there is permanent damage

how long does it take for ischemia to develop?

within 10 seconds

duration of myocardial oxygen deficit that distinguishes transient ischemia from permanent ischemia

20 minutes

stable angina

recurrent, predictable chest pain

patho of stable angina

gradual luminal narrowing and hardening of the arterial walls causing the affected vessels to not be able to dilate in response to increased myocardial demand associated with physical exertion or emotional stress

characteristics of stable angina

- reproducible (i.e., this happens every time I mow my yard, etc.)

- with rest, myocardial blood flow is restored and no necrosis of myocardial cells results

angina pectoris

chest pain caused by myocardial ischemia often characterized as transient and substernal discomfort

prinzmetal angina (variant)

causes unpredictable chest pain that often occurs at night during REM sleep

patho of prinzmetal angina

vasospasm may result from decreased vagal activity, hyperactivity of the SNS, and decreased nitric oxide activity

silent ischemia and mental stress (induced)

causes no detectable symptoms (i.e., fatigue, dyspnea, or feeling of unease)

patho of silent ischemia and mental stress (induced)

mental stress can result in the release of catecholamines and increase in HR, BP, and vascular resistance

acute coronary syndromes

sudden coronary obstruction due to thrombus formation over a ruptured atherosclerotic plaque (i.e., unstable angina, MI)

unstable angina

reversible myocardial ischemia and a harbinger of impending infarction

characteristics of unstable angina

transient episodes of thrombotic vessel occlusion and vasoconstriction occur at the site of plaque damage with a return of perfusion before significant myocardial necrosis occurs

myocardial infarction (MI)

prolonged ischemia causes irreversible damage to the heart muscle (myocyte necrosis)

characteristics of myocardial infarction

- subendocardial vs. transmural

- cellular injury leading to cellular death

- structural and functional changes

- repair

structural and functional changes seen following myocardial infarction

- myocardial stunning

- hibernating myocardium

- myocardial remodeling

myocardial stunning

the temporary loss of contractile function that persists for hours to days after perfusion has been restored

hibernating myocardium

tissue, that is persistently ischemic, undergoes metabolic adaptation to prolong myocyte survival

myocardial remodeling

process that occurs in the myocardium after an MI

repair following an MI

degradation of damaged cells, proliferation of fibroblasts, and synthesis of scar tissue

overall effects of angiotensin II following an MI

involved in myocardial remodeling as it causes myocyte hypertrophy, scarring, and loss of contractile function in the areas of the heart distant from the site of the infarction

systemic angiotensin II effects following an MI

peripheral vasoconstriction and fluid retention results in myocardial work increasing thus the effects of the loss of myocyte contractility are exacerbated

local angiotensin II effects following an MI

growth factor for vascular smooth muscle cells, myocytes, and cardiac fibroblasts promotes catecholamine release and causes coronary artery spasms

clinical manifestations of MI

- infarcted myocardium is surrounded by a zone of hypoxic injury, which may progress to necrosis or return to normal; adjacent to this zone is a zone of reversible ischemia

- sudden severe chest pain

- ECG changes (STEMI or NSTEMI)

- troponin I elevates within 2-4 hours

- creatine phosphokinase-MB, LDH

- hyperglycemia

- leukocytosis, elevated CRP seein in the repair phase

what is the most specific clinical manifestation for an MI?

elevated troponin I levels

complications of MI

- dysrhythmias

- heart failure

- cardiogenic shock

- pericarditis

- ventricular aneurysm

acute pericarditis

acute inflammation of the pericardium

patho of acute pericarditis

most often idiopathic but can be viral

symptoms of acute pericarditis

- fever, myalgia, malaise

- chest pain with movement or lying down

- sinus tachy

- friction rub (highly specific)

pericardial effusion

accumulation of fluid in the pericardial cavity

transudative pericardial effusion

- extravascular fluid, low in protein, non-inflammatory

- could be due to heart failure or overhydration

exudative pericardial effusion

- direct irritation pericardium

- inflammation, infection, malignancy, autoimmune

complications of pericardial effusion

- if fluid buildup develops rapidly, tamponade can occur

- if fluid buildup develops slowly, the pericardial sac accommodates larger amounts of fluid without compression

cardiac tamponade

fluid accumulation in the pericardium that compresses the heart

dangers of cardiac tamponade

when pressure exerted by the fluid equals diastolic pressure in the chambers (usually the right side first)

symptoms of cardiac tamponade

- JVD

- reduced cardiac output

- pulsus paradoxus

- water bottle configuration on CXR

pulsus paradoxus

arterial BP during expiration exceeds the pressure during inspiration by more than 10 mmHg

constrictive (restrictive) pericarditis

fibrous scarring with occasional calcification of the pericardium causes the visceral and parietal pericardial layers to adhere and encase the heart in a rigid shell

clinical manifestations of constrictive (restrictive) pericarditis

exercise intolerance, dyspnea on exertion, fatigue, and anorexia

cardiomyopathies

effects of neurohumoral responses to ischemic heart disease or hypertension on the heart muscle cause remodeling

patho of cardiomyopathies

many cases are idiopathic

dilated cardiomyopathy

impaired systolic function leading to increases in intracardiac volume, ventricular dilation, and systolic heart failure (thin walls)

causes of dilated cardiomyopathy

- ischemic heart disease

- valvular disease

- diabetes

- alcohol

- drug toxicity

- renal failure

- hyperthyroidism

- deficiencies of niacin, vitamin D, and selenium

- infection

clinical manifestations of dilated cardiomyopathy

dyspnea, fatigue, and pedal edema

hypertrophic cardiomyopathy

- thickening of the septal wall

- most common inherited heart defect

effects of hypertrophic cardiomyopathy

obstruction of left ventricular outflow tract (more apparent whenever heart rate increases)

clinical manifestations of hypertrophic cardiomyopathy

angina, syncope, palpitations, left heart failure, MI symptoms

hypertensive (valvular hypertrophic) cardiomyopathy

hypertrophy of the myocytes in an attempt to compensate for increased myocardial workload

patho of hypertensive (valvular hypertrophic) cardiomyopathy

long-term dysfunction of the myocytes develops over time; first diastolic dysfunction leading to systolic dysfunction of the ventricle

clinical manifestations of hypertensive (valvular hypertrophic) cardiomyopathy

- can be asymptomatic

- may complain of angina, syncope, dyspnea on exertion, and palpitations

restrictive cardiomyopathy

myocardium becomes rigid and noncompliant, impeded ventricular filling and raising filling pressures during diastole

clinical manifestations of restrictive cardiomyopathy

right heart failure occurs with systemic venous congestion

common causes of restrictive cardiomyopathy

systemic disease (think scleroderma, amyloidosis, sarcoidosis, lymphoma, etc.)

valvular dysfunction

stimulates chamber dilation and/or myocardial hypertrophy

which side is affected more by valvular dysfunction?

the left heart (mitral and aortic valves) more commonly than the right heart (tricuspid and pulmonic valves)

possible causes of valvular dysfunction

- endocardial tissue

- congenital or acquired

stenosis

- constricted, narrowed, impede forward flow

- increases workload, hypertrophy

regurgitation

- fail to shut completely

- increases blood volume/workload, leads to dilation and hypertrophy

aortic stenosis

- most common valvular abnormality

- orifice of the aortic semilunar valve narrows causing diminished blood flow from the left ventricle into the aorta

patho of aortic stenosis

- calcific degeneration related to aging (aortic sclerosis)

- congenital bicuspid valve

- inflammatory heart disease caused by rheumatic heart disease

clinical manifestations of aortic stenosis

angina, syncope, and dyspnea

mitral stenosis

impaired flow from left atrium to left ventricle

patho of mitral stenosis

most commonly caused by rheumatic disease (group A beta-hemolytic strep); autoimmune activation of lymphocytes and macrophages leads to inflammatory damage and scarring of valve leaflets

effects of mitral stenosis

- incomplete emptying of the left atrium

- chamber dilation and hypertrophy

- atrial arrhythmias

- decreased CO

aortic regurgitation

inability of the aortic valve leaflets to close properly during diastole

patho of aortic regurgitation

can be primary or secondary (i.e., from chronic HTN)

clinical manifestations of aortic regurgitation

widened pulse pressure as a result of increased stroke volume and diastolic backflow

mitral regurgitation

permits back-flow of blood from the left ventricle into the left atrium during systole

most common causes of mitral regurgitation

mitral valve prolapse, rheumatic heart disease, infective endocarditis, MI, connective tissue disease, dilated cardiomyopathy, etc.

tricuspid regurgitation

leads to volume overload in the right atrium and ventricle, increased systemic venous blood pressure, and right heart failure

mitral valve prolapse syndrome

- most common valve disorder in the U.S. and more prevalent in young women

- anterior and posterior cusps of the mitral valve billow upward ("prolapse") into the atrium during systole

clinical manifestations of mitral valve prolapse syndrome

mostly asymptomatic but a murmur may be present

patho of mitral valve prolapse syndrome

associated with Marfan, Ehlers-danlos, osteogenesis imperfecta

rheumatic fever

a diffuse, inflammatory disease caused by a delayed immune response to infection by the group A beta-hemolytic streptococci

clinical manifestations of rheumatic fever

- a febrile illness

- fever, lymphadenopathy, arthralgia, nausea, vomiting, epistaxis

if left untreated, rheumatic fever causes

rheumatic heart disease

patho of rheumatic fever

- only as a sequel to pharyngeal infection by group A beta-hemolytic strep (skin strains do not have the same antigenic molecules)

- result of abnormal humoral and cell-mediated immune response to the M proteins on the microorganisms that cross react with normal tissues

rheumatic heart disease

heart disease caused by rheumatic fever in patients with a genetic susceptibility

clinical manifestations of rheumatic heart disease

- carditis

- polyarthritis

- subcutaneous nodules

- chorea

- erythema marginatum

carditis

- inflammation of the heart

- affects primarily the valves (swelling, erosion, and vegetation of platelets and fibrin deposited on chordae tedineae)

subcutaneous nodules

develop over bony prominences and along extensor tendons of elbows, wrists, knees, and ankles

chorea

sudden aimless involuntary movements (CNS)

erythema marginatum

rash, pink, non-pruritic macules that never occur on the face or the hands

infective endocarditis

inflammation of the endocardium from infectious agents

most common causes of infective endocarditis

bacteria (especially strep, staph, and enterococci)

patho of infective endocarditis

- endocardial damage due to trauma, congenital/valvular, present of prosthetic valve

- bloodborne microorganism adherence

- formation of infective endocardial vegetations