Cardiac Pathophysiology

Meet the heart

Cardiovascular Pathophysiology

The heart is located in the mediastinum between the lungs

*Basically the heart is a 4-chambered structure that corresponds to the size of a fist.

Pericardium – anchor to diaphragm, serous membrane with fluid to lubricate
Myocardium – cardiac muscle cells
Endocardium – heart valves

*The atria are the reservoirs, think of them as filling stations and the ventricles as the pumps.

Remember the right chamber drives the blood into the low resistance pulmonary artery (1 of the great vessels) and on into the lungs.
*This is the only artery that carries deoxygenated blood.

The left ventricle is high pressure because it pushes the blood into the high resistance systemic circulation via the aorta (the other great vessel).
Remembering these basic pathways will help recognize the symptoms produced by the various abnormalities.

Also composed of an electrical system.
Conduction pathway begins at the SA node (pacemaker)
Basic rate, sinus rhythm, 70bpm
From the SA node to the atrial conduction pathways
AV node (floor of right atrium)
Through AV bundle (Bundle of His) and Purkinje network of fibers
*This conduction of impulses can be picked up by electrodes attached to skin = ECG
ECG = electrocardiogram, PQRST waves

Abnormal variations in ECG = arrhythmias
Dysrhythmias = acute problems, infarction, electrolyte imbalances

Heart rate and force of contraction controlled by cardiac control center in the Medulla
*Baroreceptors in the aorta and carotid arteries respond to SNS and PNS to alter rate

Sympathetic increases rate (tachycardia)
Parasympathetic decreases rate (bradycardia)

*Sympathetic or beta adrenergic receptors in heart site of action for beta-blockers
Beta blockers ‘fit’ the receptors so prevent SNS simulation

Factors affecting heart rate (increase)
Increased environmental temps
Exertion, exercise

*Coronary arteries supply the needs of the heart

The normal circulatory system

Cardiac cycle:
Diastole – relaxation and filling
Systole – cardiac contraction

Lubb closure of AV valves beginning of ventricular systolic (contraction)
Dubb semilunar valves close with ventricular diastole (relaxation and filling)

Murmurs – defective valves cause turbulence in flow

Pulse = heart rate
During ventricular systole (Lubb) surge of blood expands the arteries
Pulse deficit diff. between apical pulse and radial pulse

Cardiac output (CO) = volume of blood ejected by heart in 1 minute
CO = heart rate X stroke volume (volume pumped from 1 ventricle in 1 contraction)
Stroke volume varies with SNS and venous return
Cardiac reserve = ability to increase output in response to demands
Preload – amount of blood delivered to the heart by venous return
Afterload – force required to eject blood from ventricles, peripheral resistance

2 circulations:

Arteries carry blood away from the heart, elastic
Veins carry blood back to the heart, thinner walls, less smooth muscle

Blood pressure:
Pressure of blood against the systemic arterial walls
Systolic – pressure when blood ejected from left ventricle
Diastole – pressure when ventricles relaxed


Variables affecting cardiac output – viscosity, volume, venous return
Peripheral resistance – force opposing blood flow – friction, diameter, elasticity of vessel

Elevated by SNS
Antidiuretic hormone ADH - vasopressin, increases water absorption, volume
Aldosterone – increases volume by increasing reabsorption NA+ and water
Renin-angiotensin-aldosterone – initiated with a decrease in kidney blood flow

Heart disease and heart attacks

Heart disorders:
Arrhythmias, angina, heart attacks, CHF, hypertensive heart disease
Focus is on health and prevention

ECG electrocardiogram
Auscultation (murmurs)
Exercise stress tests
Chest xray films
Nuclear imaging
SPECT – CAT scan that assesses ischemia at rest
Cardiac catherization – visualize inside heart, measure pressures
Angiography – blood flow to the heart visualized
Doppler studies of peripheral pulses
Blood tests – labs for triglycerides, cholesteral, along with Na+, K+
Arterial blood gas – check O2 level and acid base balance

General treatments for cardiac:
Dietary modifications
Regular exercise
Cessation of smoking

Drug therapy –
Vasodilators (nitroglycerine),
Beta blockers,
Calcium channel blockers
Antihypertensive drugs
Adrenergic – blocking drugs
Angiotensin- converting enzyme inhibitors (ACE)
Cholesterol lowering meds

Coronary Artery Disease (CAD), Ischemic heart disease (IHD)**
Damage to the heart muscle b/c of obstruction of coronary artery
Common cause disability and death
Males develop earlier, women more complications

Arteriosclerosis all types arterial changes

Over 50, diabetic
Walls < elastic, hardens
Lumen narrows
Ischemia, necrosis – kidneys, brain, heart

What is the difference?

Arteriosclerosis, Arteriolosclerosis, and Atherosclerosis: Learn the difference between Arteriosclerosis, Arteriolosclerosis, and Atherosclerosis! Rishi is a pediatric infectious disease physician and works at Khan Academy.

Presence of atheromas (plaques)
Rough, elevated surface
Lipids, cholesterol, triglycerides synthesized in the liver
LDL low density lipoprotein (bad)
HDL high-density lipoprotein (good) want higher grades, good
Process begins with injury of the endothelial lining in artery
Causing inflammation w/ elevated CRP
Platelets adhere to damage
Lipids continue to build
Turbulent flow produces thrombus formation….

The atheroma damages cell wall, weakens, v elasticity, calcifies, bulge, rupture
Common causes of strokes, heart attacks, angina, renal disease

Modifiable or non-modifiable factors contribute

Gender (women ^ HDL till after menopause)
Genetic or familial factors

Cigarette smoking
Sedentary lifestyles
Poorly controlled diabetes
Oral contraceptives
High cholesterol and high blood pressure ^ risk of atherosclerosis, CAD

Losing weight
Lowering serum cholesterol and LDL (omega 3 fatty acids, ^ fiber, meds)
Minimize Na+ to control hypertension
Cease smoking
ASA daily, anticoagulation therapy
Surgery for atheromas, angioplasty

Angina Pectoris
Angina, chest pain, deficit of O2 to the heart muscle
Heart can adapt w/ vasodilation unless vessel walls are damaged

Chest pain patterns:
Classic, exertional
Variant vasospasm occurs at rest
Unstable angina, more serious, may precede a MI

Insufficient myocardial blood supply associated with atherosclerosis, arteriosclerosis, vasospasm
Increased demands - respiratory illness, anemia, exertion

Recurrent intermittent substernal chest pain triggered by stress and ^ demand
Pain = tightness, pressure, left arm, pallor, diaphoresis, nausea
Few seconds to minutes

Relieved by rest
Vasodilation (nitroglycerin SL) relieves vasospasm
Anti-anxiety, stress reduction
Avoiding triggers

Congestive Heart Failure:
Right or left
Affects one side first then other fails too

Right sided:
Cause: Infarction of right ventricle, pulmonary valve stenosis, pulmonary disease
Effects: decreased cardiac output, systemic congestion, edema legs, abdomen
S&S: Fatigue, weakness, dyspnea, exercise/cold intolerance
Compensation: tachycardia, pallor, polycythemia, daytime oliguria
Effects: edema feet, hepatomegaly, splenomegaly, ascites, distended neck veins, flushed face

Left sided:
Cause: infarction left ventricle, aortic valve stenosis, hypertension, hyperthyroidism
Effects: decreased cardiac output, pulmonary congestion
S&S: Fatigue, weakness, dyspnea, exercise/cold intolerance
Compensation: tachycardia, pallor, polycythemia, daytime oliguria
Effects: orthopnea, cough, SOB, paroxysmal nocturnal dyspnea, hemoptysis, rales

Arterial diseases:
Insidious onset, silent killer

3 catagories:
Primary, essential, idiopathic
Secondary, renal or endocrine origin, tumor, underlying problem must be addressed
Malignant, resistant, uncontrollable with 3 or more drugs

Hypertension = 140/90

Diastolic indicates workload of left ventricle
Mild, moderate, severe
Essential arterial vasoconstriction > decreased blood flow through kidneys > increased renin, angiotensin, and aldosterone secretion
Over time damage to arterial walls, hard, thick, sclerotic, wall may dilate, tear
Most effected kidneys, brain, retina

Increases with age
Men affected more severely
Genetic factors AA, more prevalent
High Na+
Excessive alcohol

Morning headache

Lifestyle changes
Mild diuretics
ACE inhibitors

Hypertension symptoms and categories: Learn the most common symptoms (or lack thereof!) and the two major categories of hypertension. Rishi is a pediatric infectious disease physician and works at Khan Academy.

Peripheral Vascular disease:
Any abnormality of the arteries or veins outside the heart
Most common sites of atheromas are the abdominal aorta

Increased fatigue, weakness legs
Common in legs
Defect in vein wall
Intermittent claudication leg pain associated w/ exercise
Sensory impairment – tingling, burning, numbness
Peripheral pulses weak or absent
Appearance of feet/legs change, pallor, cyanosis, skin dry, hairless, toenails thick

Doppler studies

Reduce serum cholesterol
Stop smoking
Dependent position legs
Peripheral vasodilators/calcium blockers to enhance collateral
Surgical procedures – endaterectomy
Avoid skin trauma
Treat and debride ulcers
Amputation if necessary

Aortic aneurysm
Localized dilation, weakening of aterial wall
Over time dilation enlarges, esp. if hypertension is present

Abdominal pulsating, bruit
Rupture can lead to hemorrhage and death


Varicose veins:
Deep or superficial veins
Esp. in legs


Gould, B. E., & Dyer, R. M. (2011). Pathophysiology for the health professions (4 ed.). St. Louis, Missouri: Saunders Elsevier.

Story, L. (2012). Pathophysiology: A practical approach. Sudbury, MA: Jones & Bartlett Learning .


Meet the heart

Normal circulatory system


Heart disease and heart attacks