Pathophysiology 1 - Chapter 17 and 18

Circulatory System Path

1. left sided heart chambers produce the force to propel blood through the vessels of the systemic (body) circulation

2. the left atrium receives oxygenated blood from the lungs by the way of pulmonary veins and delivers it to the left ventricle

3. the oxygenated blood is pumped by the left ventricle into the aorta which supplies the arteries of the systemic circulation

4. venous blood is collected from the capillary networks of the body and is returned to the right atrium by the way of vena cava

5. blood from the head returns via inferior vena cava

The blood supplied to the heart muscle is provided by?

coronary arteries

Two type of cardiac myocytes

• working cells

• electrical cells

Working cells

Mechanical pumping functions

Electrical Cells

Transmit electrical impulses

How does the heart utilize from ATP generated

Glycolysis and oxidative reactions

Under conditions of ATP excess, heart cells are able to store the excess ATP as

creatine phosphate (CP) by the enzyme creatine kinase (CK)

• which CK could be useful in diagnosis of myocardial infarction because it leaks into the blood stream

True or False: Both cardiac contraction and relaxation require energy

True

What are the coronary arteries involved in supplying the heart muscle?

• Right coronary artery

• Left circumflex artery

• Left anterior descending

Describe the cardiac cycle

Each heartbeat is composed of a period of ventricular contraction (systole) followed a period of relaxation (diastole)

Blood flow =

Pressure/Resistance

What are the two determinants of coronary vascular resistance

• artery diameter

• varying degrees of external compression (force) by myocardial contraction and relaxation

Coronary artery diameter is continuously adjusted to maintain

blood flow at a level adequate for myocardial demands

• vessel dilation and vessel constriction

True or False: Cardiac muscle needs a continuous supply of oxygen and nutrients to perform its pumping function

True

A disruption in cardiac blood flow (ischemia) generally results in

Some degree of pump failure and damage to cardiac tissues

Describe the determinents of stroke volume

Preload: volume of blood in the heart

Afterload: resistance to ejection from the ventricle

What is cardiac output

The amount of blood pumped out of the heart each minute

What is stroke volume?

The amount of blood ejected from the ventricle with each contraction

True or False: Coronary Heart Disease is Responsible for approx. 50% of deaths by CVD

True

What is CHD characterized by?

Insufficient delivery of oxygenated blood to myocardium caused by atherosclerotic coronary arteries

Sequelae of CHD includes

• angina pectoris (chest pain)

• myocardial infarction

• Dysrhythmias

• heart failure

• sudden cardiac death

What are known risk factors for CHD?

• ATHEROSCLEROSIS: source of nearly all CHD

• Possible microcirculation abnormalities

What does atherosclerosis cause?

Narrowing of arterial lumen that can lead to cardiac ischemia through

• thrombus formation

• coronary vasospasm

• endothelial cell dysfunction

What is defined as good and bad cholesterol?

LDL = bad cholesterol

HDL = good cholesterol

Lipid risk factors with CHD

• High total cholesterol

• High Triglycerides

• High LDL

• Low HDL

What does HDL do?

Circulates to the tissues and takes up excess free cholesterol and takes it back to the liver

What does LDL do?

It is absorbed by the tissues and 70% of it returns back to the liver

What is atherosclerotic plaque formation initiated by?

Injury to coronary artery endothelium

Vulnerable plaques

• large lipid core

• thin cap

• high shear stress

• inflammation within

Stable plaques

• more collagen and fibrin

• stable cap

LDL leakage into the vessel wall occurs with

oxidation by endothelial cells and macrophages

Oxidized lipids are damaging to

endothelial and smooth muscle cells - and stimulates recruitment of macrophages into the vessel

What accumulates within vessel wall and coalesce into lipid core?

Excess lipid and debris

Vulnerable plaques may rupture or become eroded which

stimulates clot formation on the plaque

What can ischemia result from?

Oxygen supply insufficient to meet metabolic demands

Rate of coronary perfusion can be altered by

• large, stable atherosclerotic plaque

• acute platelet aggregation and thrombosis

• vasospasm

• failure of auto regulation by the microcirculation

• poor perfusion pressure

True or False: Ischemia can result in Chronic or Acute Coronary Syndromes

True

Pathophysiology of chronic ischemia

Associated by clinical syndrome of stable angina of the coronary vessel

Pathophysiology of acute ischemia

Associated with plaque disruption (rupture) and thrombus (clot) formation which results in unstable angina or MI

Another name for unstable angina or MI

Acute coronary syndrome

True or False: Chronic or acute coronary heart syndromes may precipitate sudden cardiac arrest and associated dysrhythmias

True

Chronic coronary syndromes

• stable angina pectoris

• ischemic cardiomyopathy

Describe the chronic coronary syndromes

• both are consequence of chronic obstruction from stable atherosclerotic plaques (65-75% or more of lumen occluded)

• progresses slowly

• heart can develop alternative pathways for myocardial blood flow

True or False: Acute Coronary Syndrome is associated with acute changes in plaque morphology and thrombosis, which causes a sudden obstruction of the coronary artery

True

Acute coronary syndromes can cause an abrupt

onset and life threatening consequences

True or False: Stable angina cannot be relieved by rest

False

What factors of stable angina may upset the balance?

Factors that decrease coronary supply or increase myocardial oxygen demand can upset the balance and lead to ischemia and angina pain

Angina pectoris is chest pain associated with

Intermittent myocardial ischemia

Angina pectoris may result in inefficient

cardiac pumping with resultant pulmonary congestion and shortness of breath

True or False: No permanent myocardial damage occurs with angina pectoris

True

True or False: MI occlusion is complete and the thrombus lasts long enough to cause irreversible damage, necrosis to myocardial cells

True

Describe a stable angina

• most common

• narrow atherosclerotic coronary vessels

• coronary perfusion is inadequate during physical exertion

• onset pain is predictable and relieved by rest

Describe a prinzmetal variant angina

• initiated by vasospasm

• unpredictable attacks of pain

• some coronary atherosclerosis but symptoms are unrelated to exertion

Describe a unstable angina

• associated with acute coronary syndrome

What’s different from an unstable angina compared to an MI?

In an unstable angina - occlusion is partial, or the clot is dissolved before myocardial tissue damage

How do you accurately diagnose ACS?

Signs/symptoms, ECG changes, serum biomarkers

MI is a result of

Prolonged or total disruption of blood flow

• more than 125,000 deaths a year in the US

Nearly all infarcts (>97%) are located in the

Left ventricular walls

MI area of infarction 18-24 hours after

area becomes paler than surrounding tissues

MI area of infarction 5-7 days after

turns yellowish and soft with a rim of red vascular connective tissue

MI area of infarction 1-2 weeks after

necrotic tissue progressively degraded and cleared away; infarcted myocardium weakened and susceptible to rupture

MI area of infarction by 6 weeks

necrotic tissue replaced by tough fibrous scar tissue

Elevated levels of these biomarkers suggest leakage from fatally damaged heart cells

• myoglobin

• troponin I and T (test of choice)

• lactate dehydrogenase

• creatine kinase (CK-MB; specific for heart muscle necrosis)

What does chronic ischemic cardiomyopathy refer to?

A disorder in which heart failure develops insidiously (slowly) because of progressive ischemic myocardial damage

Treatment of ACS

• decreasing myocardial oxygen demand

• increasing myocardial oxygen supply

• monitoring and managing complications

Patients with chest pain and evidence of acute ischemia on the EKG, with a ST-segment elevation are candidates for

• Acute reperfusion therapy

Patients presenting with symptoms of unstable angina and no ST elevation on EKG are candidates for

• Clot removal and stents

• Anti-platelet drugs

• Do not benefit from reperfusion therapy

What is usually the primary cause of sudden cardiac arrest?

Lethal dysrhythmia (such as ventricular fibrillation)

Mitral valve is between which atrium and ventricle?

Valve between left atrium and left ventricle

Aortic valve is between which atrium and ventricle?

Valve allowing outflow from left ventricle to the aorta

Cardiac tissue layers (inner to outer)

endocardium → myocardium → pericardium

What is the function of the aortic valve?

Allows outflow from left ventricle to the aorta

Heart valves may be damaged by

• inflammation and scarring

• calcification

• congenital malformations

Stenosis

failure of the valve to open completely results in extra pressure work for the heart

Rerurgitation

inability of a valve to close completely results in extra volume work for the heart

Rheumatic heart disease

acute inflammatory disease that follows infection with group A beta-hemolytic streptococci

• damage by immune attack on individual’s own tissues

• mainly in children

• antibodies against the streptococcal antigens damage connective tissue in joints, heart, skin

  • causes valve swelling and damage

Describe mitral valve stenosis

• blood flow from left atrium to left ventricle impaired during ventricular diastole

• increased pressure of the left atrium leads to atrial chamber enlargement and hypertrophy

• can lead to chronic pulmonary hypertension, right ventricular hypertrophy, and right-sided heart failure

Describe mitral valve regurgitation

• back flow of blood from the left ventricle to the left atrium during ventricular systole

• left atrium and ventricle dilate and hypertrophy cause by extra volume

• may lead to left-sided heart failure

Aortic valve stenosis

• results in obstruction of aortic outflow from the left ventricle into the aorta during systole

• predominant cause is age-related calcium deposits on the aortic cusps

• left ventricle hypertrophy may result in ischemia and left-sided heart failure

Aortic valve regurgitation

• incompetent aortic valve allows blood to leak back from the aorta into the left ventricle during diastole

• caused by abnormal aortic valve or aortic root dilation

• leads to left ventricle hypertrophy and dilation with eventual left-sided heart failure

Infective endocarditis

Invasion and colonization of endocardial structures by microorganisms with resulting inflammation-vegetations

• most common bacteria: strep and staph

Acute infective endocarditis

• prognosis is poor

• intravenous drug users susceptible

Subacute infective endocarditis

• onset insidious

• risk factor for acute endocarditis

Myocarditis

Inflammatory disorder of the heart muscle characterized by necrosis and degeneration of myocytes

• caused by viruses most commonly

Myocarditis characterized by

left ventricular dysfunction (flabby with patchy or diffuse necrotic lesions) and general dilation of all four chambers

Dilated cardiomyopathy

• characterized by cardiac failure

• enlargement of one or both ventricular chambers

• reduced contractibility

Hypertrophic cardiomyopathy

• thickened hyperkinetic left ventricle

• risk of sudden cardiac arrest due to aortic flow obstructions

Restrictive cardiomyopathy

• small left ventricle volume

• stiff fibrotic left ventricle

Pericardial diseases are caused by

Accumulation of noninflammatory fluid in the pericardial sac (pericardial effusion)

Serous fluid accumulation

secondary to heart failure

Serosanguineous fluid accumulation

due to chest trauma or heart surgery

Purulent fluid accumulation

infected fluids containing WBCs

Blood accumulation

trauma

Cardiac Tamponade

When fluid accumulation in the pericardial sac is large/sudden it can lead to external compression of the heart chambers such that filling is impaired

Acute pericarditis

acute inflammation of the pericardium

• most cases idiopathic and presumed viral

Chronic pericarditis

Healing of the acute form that results in chronic dysfunction

Adhesive mediastino-pericarditis

pericardial sac is destroyed and the external aspect of the heart adheres to surrounding mediastinal structures

Constrictive pericarditis

pericardial sac becomes dense, nonelastic, fibrous, and scarred

Shunt

Abnormal path of blood flow through the heart or great vessels

• right to left: cyanotic defect

• left to right: acyanotic defect

Obstruction

interference with blood flow because of abnormal narrowing leading to increased workload of affected chamber

• acyanotic