Lecture 15-18 cardiovascular system and disorders

cardiac cycle phases

systole (contraction)

• atrial systole + ventricular systole

diastole (relaxation)

• chamber fill with blood

• ventricular diastole

atrial systole (systole)

• AV valves open and semilunar valves remain closed

• blood flows into ventricles

ventricular systole (systole)

blood ejected into pulmonary trunk and ascending aorta

2 phases:

1. Isovolumetric contraction

• All valves closed

2. Ventricular ejection

• Semilunar valves open and AV valves remain closed

diastole (relaxation)

• chambers fill with blood

• Ventricular diastole

1. Early = isovolumetric relaxation

• All valves are closed

2. Late= atria ventricles passively fill with blood

• AV valves open and semilunar valves remain closed

Ventricular systole

isovolumetric contraction + ejection period

isovolumetric contraction (ventricular systole)

begins with closure of AV valves and first heart sound (S1)

• Increased ventricular pressure

- AV and semilunar valves close and no blood leaves ventricles

ejection period (ventricular systole)

ventricular pressure is greater than aortic pressure → semilunar valves open and blood is ejected

ventricular diastole

isovolumetric relaxation + ventricular filling

isovolumetric relaxation

all valves closed and ventricular volume remains same

ventricular filling

atrial pressure is greater than ventricular pressure → AV valves open

factors affecting cardiac output

preload, afterload, cardiac contractility, heart rate

preload

degree of ventricular stretching during ventricular diastole

• related to volume of blood inside ventricle

Determine by:

• VR (venous return) - blood return

• Blood left in ventricle after systole (ESV)

Directly proportional to EDV, which depends on VR

• ↑ VR → ↑ EDV → ↑ preload → ↑ SV → ↑ CO

Afterload

pressure heart must generate to pump blood out of heart

• related to resistance to ejection during systole

systemic arterial pressure is main source of afterload work on left work

• ↑ afterload → ↑ESV  → ↓ SV → ↓ CO

cardiac contractility

determines force of contraction of cardiac muscle

• Increased force of contraction → ↓ ESV → ↑ SV → ↑ CO

• Decreased force of contraction → ↑ ESV → ↓ SV → ↓ CO

heart rate (HR)

determines frequency with which blood is ejected from heart

• ↑ HR → ↑ CO

factors affecting heart rate

• Cardioacceleratory (speeds HR) and cardioinhibitory (slows HR) centers in medulla

• Cardiovascular vasomotor control center (control of blood vessel diameter) - Sympathetic activation → ↑ HR + Parasympathetic activation → ↓ HR

• Neural reflexes - Baroreceptor reflex: when ↓ BP → ↑HR and arterioles constrict

• Hormones - Epi, NE and thyroid hormone

Vascular resistance (largest component)

due to friction between blood and vessel walls

• Vessel radius (most important)

  • Varies by vasodilation and vasoconstriction

  • ↓ vessel radius → ↑ friction → ↑ resistance

  • ↑ vessel radius → ↓ friction → ↓ resistance

Cardiac centers regulate CO

• Sympathetic nervous system stimulates cardioacceleratory center

• Parasympathetic nervous system stimulates cardioinhibitory center

• Vasomotor center regulate vessel diameter

Baroreceptor reflexes

• respond to changes in blood pressure

stretch receptors in walls of:

1. Carotid sinuses (maintain blood flow to brain)

2. Aortic sinuses (monitor start of systemic circuit)

3. Right atrium (monitors end of systemic circuit)

↑ BP, CV (cardioinhibitory) centers will:

1. ↓ CO (↓ HR and SV)

2. Cause peripheral vasodilation

↓ BP, CV (cardioacceleratory) centers will:

1. ↑ CO ( ↑ HR and SV)

2.  Cause peripheral vasoconstriction

chemoreceptor reflexes

respond to changes in chemical composition, particularly pH and dissolved gases (O2, and CO2 concentrations)

• Peripheral chemoreceptors- carotid bodies and aortic bodies

• Central chemoreceptors- within medulla oblongata

endocrine mechanisms- short-term

• Sympathetic activation

• Epi and NE from adrenal medulla ↑ CO and peripheral vasoconstriction

Antidiuretic hormone (ADH) - endocrine mechanisms

↑ BP

• Reabsorption of water from tubular fluid in collecting duct of nephron

Angiotension ll - endocrine mechanisms

Responds to ↓ renal blood pressure (renal blood flow)

Stimulates:

1. Aldosterone secretion

2. ADH secretion

3. Thirst

4. Peripheral asoconstriction

Development of ATH

1. Endothelial cell injury

2. Migration of inflammatory cells

3. Smooth muscle cell proliferation and lipid deposition

4. Gradual development of atheromatous plaque with lipid core

Fatty streaks- Types of lesions associated with ATH

• Thin, flat yellow intimal discolorations that progressively enlarge

• Consist of macrophages and smooth muscle cells that combine with lipid to form foam cells

Fibrous atheromatous plaque - Types of lesions associated with ATH

• Over time, fatty steaks grow larger and proliferate into the smooth muscle

• As lesions increase in size, they narrow lumen of artery

- Accumulation of intracellular and extracellular lipids, proliferation of vascular smooth muscle cells

This Describes Early Atherosclerosis (Plaque Formation)

• Monocytes adhere to endothelium and migrate between endothelial cells to localize in intima (innermost layer of the artery wall)

• Monocytes then transform into macrophages, which engulf lipoproteins (LDL)

• Activated macrophages release toxic oxygen species that oxidize engulfed LDL → become foam cells

Atherosclerotic plaques consist of

• Smooth muscle cells

• Macrophages, foam cells and other leukocytes

• Extracellular matrix including collagen and elastic fibers

• Intracellular and extracellular lipids

Most acute arterial occlusions are result of an:

Embolus (blood clot that moves)

• 7 P’s of acute arterial embolism

1. Pistol shot (acute onset)

2. Pallor

3. Poikilothermia (cold)

4. Pulselessness (below level of occlusion)

5. Pain

6. Paresthesia

7. Paralysis (loss of reflex and motor function)

Atherosclerotic occlusive disease (peripheral artery disease)

Sudden event that interrupts arterial flow to affected tissues or organ

• MCC: ATH

• Primary sx - Intermittent claudication (pain with walking, esp. calf pain, relieved by rest)

• Other sxs

• Atrophic changes and thinning of skin

• Foot is cool and pedal pulses are weak

Thromboangiitis obliterans (Buerger disease)

• Inflammatory (vasculitis) arterial disorder that causes thrombus formation

• Affects medium-sized arteries

• Plantar and digital vessels in foot and lower leg

• Sometimes involves hands

• Characterized by segmental, thrombosing, and acute and chronic inflammation

raynaud disease and phenomenon

• A functional disorder caused by intense (sudden tightening of the vessel wall) vasospasm of arteries and arterioles in fingers and less often toes

• Excessive vasoconstrictor response to stimuli

• because of another underlying problem

• Ischemia due to vasospasm

raynaud disease

Precipitated by exposure to cold or by strong emotions and usually is limited to the fingers

• happens by itself

varicose veins

Varicose, or (enlarged) dilated, tortuous (twisted) veins of  lower extremities

• Can lead to secondary problems of venous insufficiency•Primary varicose veins originate in superficial saphenous vein

Secondary varicose veins result from impaired flow in deep venous channels

• MCC: deep vein thrombosis (DVT)

Sxs:

• Aching in lower extremities

• Edema (swelling), especially after long periods of standing

chronic venous insufficiency

Impaired unidirectional flow of blood and emptying of deep veins → stretching of veins → rupture of valves and clot formation (thrombosis)

Etiology:

• Increased venous hydrostatic pressure (as with prolonged standing)

• Incompetent valves in veins (become weak)

• Deep vein obstructions (DVT)

chronic venous insufficiency symptoms

• Tissue congestion, edema (swelling)

• Necrosis (tissue death) of subcutaneous fat(fat under skin) deposits followed by skin atrophy (thinning/weaking)

• Brown pigmentation of skin•Impaired tissue nutrition (poor circulation

• Causes stasis dermatitis (inflammation) and development of venous ulcers (open sores)

• Stasis dermatitis = presence of thin, shiny, bluish brown, irregularly pigmented desquamative skin

• Lower leg ulcers