Pathophysiology II Exam 4 - CARDIO pt. 1

function of the right heart

- pulmonary circulation (pumps blood through the lungs)

- delivers blood to the lungs for oxygenation

- is a low pressure system

function of the left heart

- systemic circulation (pumps oxygenated blood through the body)

- is a high pressure system

arteries

carry blood away from the heart

capillaries

exchange fluids between the blood and interstitial spaces

veins

carry blood to the heart

mediastinum

area above the diaphragm and between the lungs where the heart is located

epicardium

outer smooth layer of the heart wall

myocardium

thickest layer of cardiac muscle that makes up the majority of the heart wall

endocardium

innermost layer of the heart wall

pericardium

- double-walled membranous sac that encloses the heart

- has a parietal (surface) and visceral (inner layer)

function of the pericardium

- protects and anchors the heart

- prevents overfilling of the heart with blood

- allows for the heart to work in a relatively friction-free environment

pericardial cavity

space between the parietal and visceral layers that contains pericardial fluid

chambers of the heart

right atrium, right ventricle, left atrium, left ventricle

what are the left and right atria separated by?

the interatrial septum

what are the left and right ventricles separated by?

the interventricular septum

what does the thickness of each heart chamber depend on?

the pressure or resistance it must overcome to eject blood

main function of the heart valves

ensure one-way blood flow

atrioventricular (AV) valves

one-way flow of blood from the atria to the ventricles

tricuspid valve

right AV valve that has 3 leaflets or cusps

bicuspid valve

aka "mitral valve;" left AV valve that has 2 leaflets or cusps

semilunar valves

one-way flow from the ventricles to either the pulmonary artery or to the aorta

pulmonic semilunar valve

prevents blood back-flow from pulmonary artery to right ventricle

aortic semilunar valve

prevents back-flow of blood into the left ventricle

function of the superior and inferior venae cavae

to bring deoxygenated blood from the systemic circulation to the right atrium

function of the right and left pulmonary arteries

- transport unoxygenated blood from the right heart to the right and left lungs

- branch into the pulmonary capillaries

function of the pulmonary veins

to carry oxygenated blood from the lungs to the left side of the heart

function of the aorta

to deliver oxygenated blood to systemic vessels that supply the body

cardiac cycle

one contraction and one relaxation makes up one heartbeat

diastole

relaxation

systole

contraction

path of systemic circulation

arteries -> arterioles -> capillaries -> venules -> veins

peripheral vascular system

systemic circulation that supplies the skin and the extremities

pressure affecting blood flow

force exerted on a liquid per unit area

resistance affecting blood flow

- the opposition to blood flow

- diameter and length of the blood vessels contribute to resistance (i.e., vasoconstriction/vasodilation)

- vessel radius or diameter greatly affects resistance

velocity affecting blood flow

the distance blood travels in a unit in time

viscosity affecting blood flow

thick fluids (i.e., a high hematocrit) move more slowly and cause a greater resistance to flow than thin fluids

vascular compliance affecting blood flow

- stiffness is the opposite

- the increase in volume a vessel is able to accommodate for a given increase in pressure

which blood vessels are more compliant?

veins

1 multiple choice option

mechanisms of arterial pressure regulating blood pressure

- effects of cardiac output

- neural control of resistance

- effects of hormones

- adrenomedullin

- nitric oxide, prostaglandins, endothelium-derived relaxing factor

effects of cardiac output on regulating blood pressure

cardiac output can be changed by alterations in heart rate, stroke volume, or both

neural control of resistance regulating blood pressure

- baroreceptors reduce blood pressure to normal by decreasing cardiac output and peripheral resistance

- arterial receptors (chemoreceptors) are sensitive to oxygen, carbon dioxide, or pH

effects of hormones on regulating blood pressure

- epinephrine and norepinephrine cause vasoconstriction

- ADH increases blood volume by reabsorption of water from tubular fluid in the distal tubule and the collecting duct of the nephron

- RAAS; angiotensin II vasoconstricts while aldosterone stimulates reabsorption of sodium, chloride, and water to increase blood volume and stimulate thirst

- natriuretic peptides cause loss of sodium, chloride, and water through their effects on kidney function, decreasing blood volume

adrenomedullin regulating blood pressure

powerful vasodilatory activity

nitric oxide, prostaglandins, and endothelium-derived relaxing factor regulating blood pressure

cause vasodilation

what is the leading cause of death in the United States and the world?

cardiovascular diseases

mechanisms of cardiovascular diseases

- genetic, neurohumoral, inflammatory, and metabolic

- underlying tissue and cellular alterations

varicose veins

distortion, leakage, increased intravascular hydrostatic pressure, and inflammation of the veins due to the pooling of blood

causes of varicose veins

- incompetent valves

- venous obstruction

- muscle pump dysfunction

- or a combination of these

patho of varicose veins

associated with an increase in transforming growth factor beta and basic fibroblast growth factor in vessel walls

how do varicose veins develop?

- skeletal muscle pumps blood up the vessel

- gravity pulls blood down

- overtime damages occur or the valves separate

- when valves fail, pressure increases leading to further valve failure

chronic venous insufficiency

persistent ambulatory lower extremity venous hypertension

patho of chronic venous insufficiency

venous hypertension, circulatory stasis, and tissue hypoxia lead to an inflammatory reaction in vessels and tissue

clinical manifestations of chronic venous insufficiency

- lower extremity edema

- pain

- skin changes

- necrosis

thrombosis

blood clot

deep venous thrombosis (DVT)

- detached thrombus becomes thromboembolus that can lead to pulmonary emboli

- clot in a large vein leads to obstruction of venous flow leading to increased venous pressure

- postthrombotic syndrome

Virchow's triad

- venous stasis

- venous intimal damage

- hypercoaguable state

superior vena cava (SVC) syndrome

progressive occlusion of the SVC that leads to venous distention in the upper extremities and head

leading causes of SVC syndrome

non-small cell lung cancer, small cell lung cancer, and lymphoma

clinical manifestations of SVC syndrome

- edema

- venous distention of face, neck, trunk, upper extremities

- cyanosis

- dyspnea, dysphagia, hoarseness, stridor, cough, and chest pain

- CNS changes (i.e., headache, vertigo)

- respiratory distress

hypertension

- consistent elevation of systemic arterial blood pressure

- ≥130mmHg systolic or ≥80 mmHg diastolic

isolated systolic hypertension

elevated systolic blood pressure accompanied by normal diastolic blood pressure

primary (essential) hypertension

no identifiable cause; develops over years and most likely attributed to genetic and environmental factors

secondary hypertension

caused by altered hemodynamics from an underlying primary disease or drugs

general characteristics of hypertension

- affects the entire cardiovascular system

- increases the risk for MI, kidney disease, and stroke

risk factors for hypertension

- positive family history

- advancing age

- female >70 y/o and male > 55 y/o

- African American race

- increased sodium intake

- glucose intolerance (DM)/insulin resistance

- heavy alcohol use

- obesity

- cigarettes

patho of hypertension

- increases in cardiac output (i.e., increased HR, SV, blood volume, etc.)

- increase in total peripheral resistance (i.e., increased blood viscosity, reduced vessel diameter, etc.)

patho of primary hypertension

- extremely complicated interactions of genetics and the environment mediated by neurohumoral effects (genetics interact with diet, smoking, age, and other risk factors to cause chronic changes in vasomotor tone and blood volume)

- overactivity of sympathetic nervous system and RAAS, as well as alterations in natriuretic peptides

- inflammation, endothelial dysfunction, obesity-related hormones, and insulin resistance

overactivity of RAAS

- salt and water retention leads to increased vascular resistance

- angiotensin II enhances sympathetic neural outflow and alters the release of hormones that contribute to endothelial dysfunction, insulin resistance, dyslipidemia, and platelet aggregation

- arteriolar remodeling

- associated with end organ effects of HTN

inflammation causing hypertension

- caused by endothelial injury and tissue ischemia

- release of vasoactive cytokines result in vascular remodeling, decreased production of nitric oxide (vasodilators), and increased production of endothelin (vasoconstrictors)

obesity causing hypertension

- release of leptin and adiponectin (adipokines)

- increased activity of the SNS and RAAS

- causes inflammation, small artery remodeling, endothelial dysfunction, and insulin resistance

natriuretic peptides

ANP, BNP, CNP, and urodilantin work to decrease blood pressure

dysfunction of natriuretic peptides

- leads to shift in pressure-natriuresis relationship resulting in an increased blood volume and pressure

- linked to cardiovascular remodeling

- with inadequate function, there is a compensatory increase in levels

patho of secondary hypertension

- caused by systemic disease that raises peripheral vascular resistance and/or cardiac output

- examples include renal vascular or parenchymal disease, adrenocortical tumors, adrenomedullary tumors (pheo), and drugs (such as OCPs, corticosteroids, antihistamines)

complicated hypertension

hypertrophy and hyperplasia with associated fibrosis of the tunica intima and media in a process called vascular remodeling (essentially causing ischemia)

malignant hypertension

aka "hypertensive crisis;" rapidly progressive hypertension

clinical manifestations of malignant hypertension

- diastolic pressure is usually >140 mmHg

- can lead to encephalopathy

clinical manifestations of hypertension

aka "silent disease;" early stages of hypertension have no clinical manifestations other than elevated blood pressure

diagnosis of hypertension

measurement of blood pressure on at least two separate occasions averaging two readings at least two minutes apart with the individual seated, the arm supported at heart level, after 5 minutes of rest, with no smoking or caffeine intake in the past 30 minutes

orthostatic (postural) hypotension

decrease in the systolic and diastolic blood pressures on standing by 20 mmHg or more and by 100 mmHg or more, respectively

patho of orthostatic hypotension

lack of normal blood pressure compensatory mechanisms in response to gravitational changes on the circulation, leading to pooling and vasodilation

what might cause secondary orthostatic hypotension?

medications, starvation, dehydration, immobilization, etc.

clinical manifestations of orthostatic hypotension

fainting upon standing

aneurysm

local dilation or outpouching of a vessel wall or cardiac chamber

true aneurysms

- involvement of all three layers of the arterial wall

- circumferential and saccular subtypes

false aneurysms

leak between a vascular graft and a natural artery

patho of aneurysm

constant stress on the vessel wall such as

- chronic inflammation activates matrix degrading proteins and smooth muscle apoptosis, transmural infiltration of inflammatory cells

- hypertension results in mechanical and shear forces that contributes to remodeling and weakening

- atherosclerosis and plaque formation erodes the vessel wall

clinical manifestations of a heart aneurysm

includes dysrhythmias, heart failure, and embolism of clots to the brain or other vital organ

clinical manifestations of an aortic aneurysm

asymptomatic until it ruptures, then it becomes painful (often "tearing")

clinical manifestations of a thoracic aneurysm

dysphagia and dyspnea caused by the pressure

clinical manifestations of an abdominal aneurysm

flow to an extremity is impaired, causing ischemia

aortic dissection

- a devastating complication that involves the aorta (ascending, arch, or descending)

- can disrupt flow through the arterial branches

- a surgical emergency

patho of aortic dissection

when there is inflammation and release of enzymes that damage the vessel wall followed by a tear in the intima and blood enters the wall of the artery

type A aortic dissection

involves ascending aorta

type B aortic dissection

involves descending aorta

arterial thrombus formation

activation of the coagulation cascade caused by inflammation and roughening of the tunica intima by atherosclerosis

things that can cause or be caused by arterial thrombus formation

- anatomic changes of an artery

- valvular thrombi

- shock

potential threats to circulation due to arterial thrombus formation

- thrombus may grow large enough to occlude the artery causing ischemia

- thrombus may dislodge becoming a thromboembolus that travels through the vascular system until it occludes flow into a distal systemic vascular bed

embolism

bolus of matter circulates in the bloodstream and then lodges, obstructing blood flow

arterial thrombi affect which side more?

left

1 multiple choice option

what can an embolism be?

- dislodged thrombus (often a DVT)

- air bubble

- amniotic fluid

- aggregate of fat, bacteria, cancer cells

- foreign substance