cv Flashcards
blood flow through the heart
unoxygenated blood: superior/inferior vena cava right atrium right AV (tricuspid) valve right ventricle pulmonary (semilunar) valve pulmonary arteries (to lungs) oxygenated blood: pulmonary veins (from lungs) left atrium mitral (left AV) (bicuspid) valve left ventricle aortic (semilunar) valve aorta
signs and symptoms of left sided heart failure
SOB/DOE crackles/rales at bases tachypnea diaphoresis weight gain fatigue extra heart sounds mental status changes capillary refill >3 seconds
pathway of left sided heart failure
ineffective left ventricular contractility
failure of left ventricular pumping ability
decreased cardiac output to body
blood backup into left atrium and lungs
pulmonary congestion, dyspnea, activity intolerance
pulmonary edema and right sided heart failure
signs and symptoms of right sided heart failure
hepatomegaly splenomegaly ascites dependent pitting edema JVD weight gain anorexia extra heart sounds
pathway of right sided heart failure
ineffective right ventricular contractility
failure of right ventricular pumping ability
decreased cardiac output to lungs
blood backup into right atrium and peripheral circulation
weight gain, peripheral edema, engorgement of kidneys and other organs
definition of left sided heart failure
When the left ventricle of the heart no longer pumps enough blood around the body, and blood builds up in the pulmonary veins causing shortness of breath, trouble breathing or coughing – especially during physical activity. The most common type producing signs of pulmonary congestion including crackles, S3 and S4 heart sounds and pleural effusion. Pulmonary circulation is impacted resulting in tachypnea, orthopnea, wheezing pulmonary edema.
definition of right sided heart failure
When the right ventricle of the heart is too weak to pump enough blood to the lungs blood builds up in the veins. The increased pressure inside the veins pushes fluid out of the veins into surrounding tissue leading to a build-up of fluid in the legs, or less commonly in the genital area, organs or the abdomen (belly). Venous congestion in the systemic circulation results in JVD and ascites (from vascular congestion in the GI tract) and hepatomegaly, splenomegaly, peripheral edema.
biventricular heart failure
Both sides of the heart are affected causing many of the same symptoms as both left-sided and right-sided heart failure, such as shortness of breath and a build-up of fluid.
Left-sided heart failure – usually caused by coronary artery disease (CAD), a heart attack or long-term high blood pressure.
Right-sided heart failure – usually develops as a result of advanced left-sided heart failure, or is sometimes caused by high blood pressure in the lungs, pulmonary embolism, or certain lung diseases such as COPD
aorta
the largest artery in the body
dissection of aorta
aortic vessel wall weakens and splits
aneurysm (dilation) of aorta
aortic vessel wall weakens and bulges and can rupture
acute and chronic dissection and aneurysm of aorta
Acute - Usually undetectable until dissection or rupture
Chronic – Close monitoring if family history prior to acute presentation
Chronic – When operation can be delayed following onset of acute symptoms
three types of aortic aneurysms
abdominal aortic
thoracic
thoracic abdominal
physical exam and diagnostic tests for aortic dissection and aneurysm
chest x ray
ct scan
mri
ultrasound
factors that increase risk of aortic aneurysm rupture
Connective tissue disorders Diabetes High blood pressure and cholesterol Lack of physical activity Obesity Smoking
lifestyle adjustments to prevent aortic aneurysm rupture
Eat a heart-healthy diet
Manage stress
Get regular exercise
Quit smoking
surgery for aortic aneurysm
Not all weakened or bulging vessels require immediate surgery
Aneurysms are rated by size — the larger the aneurysm the greater chance it will rupture
If the aortic vessel ruptures, immediate surgery is vital
Lifestyle changes and medications for prevention
Surgery - to replace or repair the damaged area
patient presentation with aortic aneurysm rupture
Similar to heart attack Chest, abdominal, back, neck or jaw pain Clammy skin Difficulty breathing Dizziness Fainting Feeling weak on one side of your body Hoarse throat Nausea/vomiting
the health of the cv system is important for
the health of all the other body tissues and existence of the organism as a whole
Maintains homeostasis
Delivers oxygenated blood to all tissues in the body
Removes wastes
aging and decline of the cv system can lead to
to increase in cardiovascular diseases including atherosclerosis, hypertension, myocardial infarction, and stroke
pathological alterations in cv system with aging
alterations include hypertrophy, altered left ventricular (LV) diastolic function, and diminished LV systolic reverse capacity, increased arterial stiffness, and impaired endothelial function
structural changes to cv system with aging
Pathological alterations resulting from aging CV tissues include hypertrophy, and arterial stiffness
Loss of Sinoatrial node [SAN] cells
functional changes to cv system with aging
decreased ability to respond to increased workload
cardio-protection and repair process changes to cv system with aging
decreased ability to respond to injury
Increase cardiovascular disease incidence and prevalence:
Including atherosclerosis, hypertension, myocardial infarction, stroke
Systemic disease and age-associated changes to other organ systems affect cardiac structure and function
age related changes in vascular structure and function
Thickening and stiffening of large arteries
Due to increased collagen and calcium deposition, and loss of elastic fibers in media
Cause systolic BP to rise and diastolic BP to decrease
age related changes in cv function
Elevated systolic blood pressure with declining diastolic BP leads to increased pulse pressure
Increased left ventricular wall thickness due to cellular hypertrophy – no change in cavity size
Reduced early diastolic filling
Impaired cardiac reserve
Alterations in heart rate rhythm:
Heart rate changes due to SAN cell loss, fibrosis, hypertrophy which slow propagation of electric impulse through the heart
Prolonged cardiac action potential – slowed AP firing rates
age related cv changes impact on renal system
Heart-Kidney Function: Cardiorenal syndrome
Decline in renal function contributes to improper maintenance of extracellular fluid volume and composition –unable to clear waste and water – potential increase in fluid and increase in BP
Decline in cardiac function can lead to decreased blood flow which impedes kidney capability to clear waste – potential damage to kidneys
morphological changes to cv system with aging
progressive loss of elasticity of large arteries
generalized hypertrophy of the left ventricular wall
fibrotic changes and diminished elasticity of heart muscle (reduced myocardial compliance)
reduced compliance of LVEF
cardiac output maintained by increasing end-diastolic volume
functional changes to cv system with aging
increased systolic blood pressure
increased afterload for the left ventricle
increased left ventricular end-diastolic volume
volume sensitive and volume intolerant cv system
inability to optimally respond to stress (cannot significantly increase LVEF)
increased stroke volume
decreased muscle tone results in
Decreased tissue oxygenation related to decreased cardiac output and reserve
increased heart size, left ventricular enlargement results in
compensation for decreased muscle tone
decreased cardiac output results in
Increased chance of heart failure; decreased peripheral circulation
decreased elasticity of heart muscle and blood vessels results in
Decreased venous return; increased dependent edema; increased incidence of orthostatic hypotension; increased varicosities and hemorrhoids
decreased pacemaker cells results in
Heart rate 40–100 beats per minute; increased incidence of ectopic or premature beats; increased risk for conduction abnormalities
decreased baroreceptor sensitivity results in
Decreased adaptation to changes in blood pressure
increased incidence of valvular sclerosis results in
increased risk for heart murmurs
increased atherosclerosis results in
increased blood pressure, weaker peripheral pulses
assess apical and peripheral pulses
Observe closely for abnormal sounds; determine presence and strength of peripheral pulses comparing both sides of the body. When assessing lower extremities, start distally and move toward trunk.
assess blood pressure lying, sitting, and standing
Hypotension is likely to occur while changing position; encourage patient to change positions slowly and to seek assistance if dizzy
assess ability to tolerate activity
instruct patient to rest if short of breath or fatigued
hypertension
bp consistently >140/90 mmHg
exception for people with chronic kidney disease or diabetes 130/80 mmHg
hypertension associated with
increased risk for target organ disease events– such as MI, kidney disease and stroke
isolated systolic hypertension
systolic >130 mmHg with normal diastolic
Common in people >65 years of age
Develops as a result of reduced elasticity of the arterial system
Some contributors to artery stiffness: ageing, hyperthyroidism, diabetes
Leads to increased risk of stroke, heart disease, chronic kidney disease
prehypertension
systolic = 120-139
or
diastolic =80-89
stage 1 hypertension
systolic = 140-159
or
diastolic = 90-99
stage 2 hypertension
systolic = >160
or
diastolic = >100
primary hypertension
Majority of HTN cases ~ 95%
HTN caused by increases in cardiac output (CO) or total peripheral resistance, or both
CO increases by increase in HR or stroke volume (SV)
Peripheral resistance increases with increased blood viscosity or reduced vessel diameter
Specific cause of primary hypertension unknown
primary hypertension risk factors
Family history Advancing age Cigarette smoking Obesity Heavy alcohol consumption Gender (male < 55, women > 55) Black race High dietary sodium intake Low dietary intake of potassium, calcium and magnesium Glucose intolerance
primary hypertension patho
Interaction between genetics, an increase in vascular tone and changes in blood volume cause a sustained increase in blood pressure
Pathogenesis of primary hypertension include:
SNS
Renin-Angiotensin –Aldosterone System
Natriuretic Peptides modulate renal sodium
Inflammation due to endothelial injury and tissue ischemia
Obesity
Insulin resistance
natriuresis
Natriuresis: The excretion of sodium by the kidneys, which is controlled in large part by atrial natriuretic peptide (ANP).
ANP may increase the glomerular filtration rate by binding to ANP receptors on glomerular mesangial cells, causing them to relax, thereby increasing the effective surface area available for filtration.
pressure natriuresis
Dominant physiological mechanism that connects changes in the systemic arterial pressure to changes in total body sodium amount.
pressure natriuresis acts by
increasing renal sodium excretion when incoming arterial pressure to the kidneys rises.
Autonomous within the kidneys and independently of any external neurohormonal regulatory mechanisms.
Connects renal sodium transport to arterial
Dominant mechanism of both ECF Volume Regulation and Systemic Arterial Pressure - Long-term Regulation.
signs and symptoms of htn
Usually asymptomatic If BP high may have: Headache Dizziness, fatigue Vision problems Epistaxis Chest pain 4th heart sound hematuria
diagnostic tests for htn
Multiple BP measurements to confirm
Urinalysis, urine albumin:creatinine ratio
Blood tests: fasting lipids, creatinine, potassium, sodium, TSH, fasting glucose
ECG
secondary hypertension
Caused by an underlying disease process or medication that raises peripheral vascular resistance or cardiac output
pathogenesis of secondary hypertension by cause
Renal Disorders Endocrine Disorders – eg. Diabetes Vascular Disorders Pregnancy Induced Hypertension (PIH) Neurological Disorders Acute Stress Drugs and other Substances
what does the cv system consist of
heart
blood vessels
blood
lymphatic system
