Circulatory System

Systole

period where ventricles contract

Diastole

period where ventricles relax and fill with blood

Pulmonary circulation

moves deoxygenated blood through lungs where gas exchange occurs

Systemic circulation

moves oxygenated blood to other tissues

Stenosis

Narrowing of valve that obstructs blood flow

Regurgitation

Valve doesn’t close fully, causing blood to backflow

Valve prolapse

Valve leaflets bulge backwards (usually into an atrium) due to weakness → causes regurgitation

Right sided HF

Blood flows back into body/systemic circulation (veins) → peripheral edema, JVD, weight gain, ascites

Left sided HF

Blood flows back into lungs → pulmonary congestion (crackles, cough, dyspnea), orthopnea, fatigue, weakness, ↓ CO

Preload

amount of blood filling the ventricles at end-diastole (EDV)

Afterload

resistance ventricles must overcome to eject blood (pressure)

Stroke volume

volume of blood the heart pumps out each beat (squeezing)

Normal Ejection Fraction

50%-70%

Frank-Starling Law

The more the heart stretches, the stronger it contracts and jects more blood

Compliance of Heart

The ease at which the heart expands during filling; fills more easily and stretches better = ↑ CO

Inotropes

Increases the contractility of heart → stronger squeeze → ↑ SV and CO

Beta blockers

Decreases heart rate to give ventricles more time to fill → ↑ SV and oxygen delivery (more efficiency)

Blood pressure formula

CO x peripheral vascular resistance (PVR)

What is PVR controlled by?

Stretch-sensitive baroreceptors regulate PVR to maintain BP and tissue perfusion by vasoconstricting or vasodilating

Low BP

Too low causes poor tissue perfusion → inadequate oxygen and nutrient delivery, buildup of waste

High BP

Too high damages vessel endothelium → promotes atherosclerosis and risk of vessel rupture

Risk Factors for Hypertension

Age, gender/race, family hx, diet (sodium), smoking, alcohol, obesity

Organs affected by HTN

Heart, brain, peripheral vascular, kidneys, eyes

Orthostatic hypotension

Decreased systolic BP (>20mmHg) OR decreased diastolic BP (>10mmHg) within 3 minutes of standing or 60* tilt

Causes of Orthostatic Hypotension

Fluid deficit, medications, aging, ANS dysfunction, immobility

Pericardium

Fibrous sac around the heart that keeps heart in fixed position and protects it physically

Myocardium

Muscular layer forming the walls of ventricles and atria responsible for contraction (intercalated discs)

Endocardium

Thin, three-layered inner membrane lining of heart with smooth surface for blood flow and valve function

Pericardial Effusion

Fluid accumulation in the pericardial cavity (asymptomatic or can cause complications)

Cardiac tamponade

Fluid in pericardial sac compressing the heart —> impairing proper relaxation of heart —> low CO —> hypotension and tachycardia (compensation)

Pericarditis

Inflammation of the pericardiac sac (acute, chronic, or obstructive; can impair heart function if severe)

Coronary Heart Disease

Impaired coronary blood flow leading to oxygen deprivation of heart

Causes of CAD

Angina, MI, cardiac arrhythmias, conduction defects (electrical), HF, cardiac arrest/death

Myocardial Infarction (MI)

Irreversible death of heart muscle due to prolonged lack of blood flow (complete blockage)

Cardiac arrhythmias

Electrical misfiring causing irregular rhythm

Angina

Ischemia causes chest pain

Electrocardiogram (ECG)

Detects changes in pattern in electrical activity that indicates ischemia or infarction

Echocardiogram (ultrasound)

Uses sound waves to visualize heart structure and blood flow (identifies wall motion abnormalities and valve function)

Ways to view coronary blood flow and myocardial perfusion

Electrocardiogram, echocardiogram, stress testing, nuclear cardiovascular imaging methods

STEMI

Full thickness infarction (heart muscle dmg) with ST elevation on ECG indicating complete coronary artery blockage

Manifestations of STEMI

Abrupt onset with severe and crushing chest pain, NV, fatigue, tachycardia (restlessness, impending doom feeling), pale skin

NSTEMI

Partial coronary artery blockage w/ no ST elevation and only partial muscle damage (subendocardial)

Cardiac Arrest

Disruptions in electrical activity causes heart to stop beating, so no blood goes to brain or body

Causes of Cardiac Arrest

-Asystole — no electrical activity

-Ventricular fabulation — ventricle quivers uncontrollably (no coordinated contractions); bottom chambers (fatal)

-Ventricular tachycardia — ventricle beats too fast → filling and SV continually decrease → no CO

Atrial Fibrillation (A-fib)

Atria quivers instead of contracting effectively, causing irregular and fast heartbeat; increases risk of clots (top chamber)

Chemoreceptors

Monitors blood O2, CO2, and pH to adjust respirations and circulations (triggers sympathetic if O2 too low)

Atherosclerosis

Fatty plaques integrating into arterial walls causing narrow arteries and reducing blood flow

Cause of Atherosclerosis

Endothelial injury lets LDL enter vessel wall, triggering inflammation and macrophages that form fatty streaks that promote and grow plaques

Low-density Lipoprotein

Main carrier of cholesterol; can deposit in arterial walls (atherosclerosis)

High-density Lipoprotein

Removes cholesterol from tissues and carries to liver for elimination (about 50% of proteins)

Hypercholesterolemia

Serum cholesterol >200mg/dL; can cause atherosclerosis, MI, stroke, HF

Seven P’s of Acute Arterial Embolism

Pistol shot (acute onset), pallor, polar, pulselessness, pain, paresthesia, paralysis

Aneurysms

Abnormal localized dilation of veins or arteries that can be at risk for rupture

Venous stasis

Impaired venous return causes tissue congestion and stagnant blood flow, increasing clot formation

Varicose veins

Weak or damaged vein valves causing blood to pool, making veins enlarged and twisted

Thrombophlebitis

Blood clots in a vein that causes inflammation

Risk Factors Associated with Venous Stasis

Bed rest, immobility, spinal cord injury, acute MI, congestive HF, stroke, venous obstruction

Deep Vein Thrombosis

Damaged or deformed valve leaflets in deep veins, especially in leg

Vein Valves

One-way flaps in veins that keep blood flowing toward the heart and preventing backflow

Venous Ulcers

Blood pooling → ↑ venous pressure → fluid/RBC leakage → brown skin, stasis dermatitis, edema, poor oxygen → skin breakdown.