Pathophysiology: Cardiovascular System

high output failure

- inability of heart to supply body with blood-borne nutrients despite adequate blood volume and normal or elevated myocardial contractility
- metabolic needs aren't being met0

shock

- cardiovascular system fails to perfuse the tissues adequately
- rapid decrease in BP
- impaired oxygen use
- impaured glucose use
- aerobic --> anaerobic respiration

cardiogenic shock

- decreased cardiac output
- normal vascular blood volume

hypovolemic shock

- decrease in vascular blood volume
- fluid --> interstitial space --> vascular space

neurogenic shock

- any factor that inhibits sympathetic nervous system (spinal shock)

anaphlactic shock

- allergic reactions
- exposure to allergen

septic shock

- infectious organism in blood
- bacleriemia

multiple organ dysfunction syndrome

- progressive dysfunction of 2 or more organ systems
- result from an uncontrolled inflammatory response to severe illness or injury

pulmonary circulation

right heart"
pumps blood thru lungs

systemic circulation

left heart"
pumps blood to entire body (everything except lungs)
contains oxygenated blood

mediastinum

what makes up the heart
area above diaphragm and between lungs

heart wall

encloses heart and divides it into chambers
pericardium, myocardium, endocardium

pericardium

outer layer of the heart
prevents displacement
protects against infection
2 layers: parietal and visceral
pericardial cavity and fluid

myocardium

thickest; muscular layer of heart

endocardium

innermost layer of heart
contractile force

interventricular septum

separates right and left sides of heart
prevents blood from crossing

chambers of the heart

right atrium, left atrium, right ventricle, left ventricle

valves of the heart

atrioventricular (tricuspid and mitral) & semi-lunar (pulmonic and aortic)

atrioventricular valves

1. tricuspid valve: right heart
2. mitral valve: left heart

semi-lunar valves

open when pressure is increased; blood flows into circulation
close to prevent backflow
1. pulmonic valve (right heart)
2. aortic valve (left heart)

superior and inferior vena cava

great vessel
right heart
enter right atrium

pulmonary artery

great vessel
from right ventricle; enters pulmonary circulation
divide into right and left PA
transport deoxygenated blood

pulmonary veins

great vessel
carry oxygenated blood
from lungs to left atrium

aorta

great vessel
pumps blood to entire body

right heart blood flow

superior vena cava
right atriu
triscupid valve
right ventricle
pulmonary valve
pulmonary artery
lungs

left heart blood flow

lungs
pulmonary veins
left atrium
mitral valve
left ventricle
aortic valve
aorta
entire body

cardiac cycle

diastole and systole

diastole

relaxation
occurs when AV valves open
blood fills ventricles
capillary perfusion

systole

contractoin
ventricles contract
propels blood of pulmonary artery and aorta
AV valves close

coronary vessels

support metabolic needs of the heart
go across myocardium
right: extends around right heart to posterior
left: circumflex artery - provides blood to left atrium

coronary vessel flow

coronary arteries
collateral arteries
coronary capillaries
coronary veins (coronary sinus, great cardiac vein, posterior vein of LV)
coronary lymphatic vessels

collateral arteries

supply blood/O2 to myocardium

coronary capillaries

exchange O2 and nutrients

coronary lymphatic vessels

fluid to lymphnodes

cardiac action potentials

electrical impulses that travel thru myocardium

conduction system

special cells enable myocardium to transmit action potentions
SA node, AV node, Bundle of His, R/L Bundle Branches, Purkinje Fibers

sinoatrial node

primary pacemaker

atrioventricular node

conduction between atria and ventricles

bundle of his

AV bundle; gives rise to right and left bundle branches

purkinje fibers

terminal branches of RBB and LBB`

absolute refractory period

no new action potential can be initiated
follows depolarization

cardiac performance

heart rate x stroke volume
volume increases, cardiac output increases
preload and afterload

preload

left ventricular end-diastolic volume
frank-starling law of heart

frank-starling law of heart

direct relation between volume of blood in heart and force of contraction

afterload

resistance to ejection of blood from left ventricle
the load the muscle must move after it starts to contract

heart rate

speed of cardiac cycle
affected by: cardiovascular control center, neural reflexes, atrial receptors, hormones and biochemicals

medulla

cardiovascular control center
affects heart rate

neural reflexes

affects heart rate
bainbridge (increase) and baroreceptor (decrease)

atrial receptors

sits on atria and affects heart rate

hormones and biochemicals

affects heart rate
epinephrine (increase heart rate)
ecetocoline (decrease heart rate)

myocardial contracility

squeeze of heart", affected by:
stroke volume: L's of blood ejected from heart with each beat
inotropic agents: improve contracility of heart
O2 and CO2 levels

cardiac output

volume of blood flowing through systemic/pulmonary circuit in liters/min
heart rate x stroke volume
normal adult: 5L/min

systemic circulation

left heart; to entire body:
arteries
arterioles
capillaries
venules
veins

endothelium

lining of blood vessel
innermost
resistance to blood flow is related to diameter

lymphatic system

important for fluid balance
special vascular system that picks up excess fluid and returns it to bloodstream
flows: lymphatic fluid (H2O and dissolved proteins) to lymphatic veins/venules to right lymphatic duct to thoracic duct to afferent/efferent lymph

varicose veins

vein in which blood has pooled
distented, tortuous and palpable veins
"pertrude" thru skin
causes: trauma or gradual venous distention; long periods of standing

chronic venous insufficiency

inadequate venous return over a long period due to varicose veins or valvular incompetence
venous statis ulcers (cell death and necrosis)

deep venous thrombosis

disease of veins
thrombus
obstruction of venous flow leading to increased venous pressure
factors: Triad Virchow (venous stasis, venous endothelial damage, hypercoaguble states)

thrombus

blood clot attached to vessel wall

thromboembolis

detached/traveling blood clot

superior vena cava syndrome

progression occlusion of SVC that leads to venous distention of upper extremities and head
oncologic emergency

primary hypertension

0

prehypertension

121-139 or 80-89 BP
stage 1: >140-159 or >90-99
stage 2: >160 or >100

end-organ damage

other organs begin to shut down because of untreated hypertension

secondary hypertension

BP elevation caused by a systemic disease process that raises peripheral vascular resistance or cardiac output

isolated systolic hypertension

elevations of systolic pressure are caused by increase in cardiac output, total peripheral vascular resistance or both

complicated hypertension

chronic hypersensitive damage to walls of systemic blood vessels
smooth muscle cells undergo hypertrophy and hyperplasia with fibrosis of tunica intima and media

malignant hypertension

rapidly progressive hypertension
diastolic pressure usually >140 mm Hg

orthostatic hypertension

postural"
decrease in both systolic and diastolic blood pressure upon standing
SYNCOPE
lack of normal blood pressure compensation in response to gravitational changes on the circulation
acute vs. chronic
syncope and fainting

aneurysm

disease of arteries/veins
local dilation or outpouching of a vessel wall or cardiac chamber

thrombus formation

blood clot that remains attached to vessel wall
thromboembolus
thrombophlebitis
arterial
venous

embolism

bolus of matter that circulates in the bloodstream
*dislodged thrombus, air bubble, amniotic fluid, aggregate of fluid, bacteria, cancer cells, or foreign substance

peripheral artery disease

artheroslerotic disease of the arteries that perfuse the limbs
intermittent claudication
*arteriosclerosis: abnormal thickening/hardening of vessel walls

arteriosclerosis

chronic disease if arterial system
abnormal thickening/hardening of vessel walls
plaque formation of lipid macrophages
smooth muscle cells and collagen fibers migrate to tunica intima

artherosclerosis

form of of arteriosclerosis
thickening caused by accumulation of lipid macrophages in arterial wall
plaque development

raynaud disease

peripheral artery disease
episodic vasospasm in arteries/arterioles of fingers, less commonly toes
primary vasospastic disorder with uknown origin
sensitive to cold and prolonged exposure to vibration
reversible
lack of good blood supply
secondary to othe

coronary artery disease

any vascular disorder that narrows/occludes the coronary arteries
most common cause: artherosclerosis
risk factors: dyslipidemia (increased lipid/fat level); hypertension; smoking; diabetes; obesity/sedentary lifestyle

myocardial ischemia

coronary artery disease; "heart attack"
local, temporary deprivation of coronary blood supply
stable angina, prinzmetal angina, silent ischemia (no symptoms)
fibrous plaque leads to angina (chest pain)

stable angina

current chest pain; can be reversible

prinzmetal angina

variable chest pain; occurs at rest (unpredictable)

transient ischemia

acute coronary syndrome
comes and goes

unstable angine

acute coronary syndrome
impending myocardial ischemia (heart attack)

sustained ischemia

acute coronary syndrome
irreversible; is a heart attack

myocardial infarction

acute coronary syndrome
prolonged ischemia causing irreversible damage
STEMI (ST elevation) or non-STEMI

myocardial infarction

sudden and extended obstruction of myocardial blood supply
subendocardial infarction - beneath endocardiu
transmural infarction - all 3 layers
cellular injury, cellular death, structural and functional changes (myocardial stunning and remodeling) and repa

acute pericarditis

disorder or pericardium
acute inflammation
severe chest pain, fever, increased heart rate

pericardial effusion

disorder or pericardium
fluid in pericardial space

tamponafe

disorder of pericardium
result of pericardial effusion
excessive fluid leading to heart compression
life-threatening

constrictive pericarditis

disorder of pericardium
fibrotic
encases heart in hard, rigid type shell

cardiomyopathies

disorder of myocardium
dilated/congestive: systolic dysfunction
hypertrophic: thickening; increased size of cells
restrictive: decreased ability to fill chambers with blood

valvular dysfunction

disorder of endocardium
v. stenosis, v. regurgitation, mitral valve prolapse

valvular stenosis

disorder of endocardium
shrinking/narrowing of aortic or mitral valves

valvular regurgiation

disorder of endocardium
backflow of blood into aortic, mitral or tricuspid valves

mitral valve prolapse

disorder of endocardium
cusps billow upward into left atrium

rheumatic fever and heart disease

diffuse inflammatory disease caused by a delayed immune response to infection by group A beta-hemolytic streptococci
febrile illness: inflammation of joints, skin, nervous system and heart
left untreated --> rheumatic heart disease (esp. right heart)
valv

ineffective endocarditis

inflammation of endocardium
agents: bacteria, viruses, fungi, rickettsiae, parasites
pathogenesis: 1. "prepared" endorcardium (damaged) 2. adherence of blood-borne microorganism 3. proliferation/growth of microorganism

dysrythmias

disturbance of heart rhythm
range: occassional "missed" or rapid beats to severe disturbances that affect the pumping ability of the heart
caused by: abnormal rate of pulse generation or abnormal pulse conduction

tachycardia

dysrhythmia
fast heart rate
100-150 BPM
exercises, septic shock, blood loss

flutter

dysrhythmia
fast hear rate
>250 BPM

fibrillation

dysrhythmia
fast; >300 BPM
can lead to cardiac arrest

bradycardia

dysrhythmia
slow; <150 BPM

asystole

without heart rate
0 BPM
cardiac arrest

heart failure

several types of cardiac dysfunction that result in inadequate perfusion of tissues with blood borne nutrients
right and left, high output failure

left heart failure

congestive"
systolic: inability of heart to generate adequate cardiac output to perfuse tisues
diastolic: pulmonary congestion despite normal stroke volume and cardiac output

right heart failure

common cause: diffuse hypoxic pulmonary disease
can result from increase in left ventricular filling pressuer that's reflected back into the pulmonary circulation
more respiratory symptoms