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
what are the functions of the cv system
Transport of nutrients, oxygen and hormones throughout body
Removal of metabolic wastes [nitrogen, carbon dioxide]
Protection of the body as the white blood cells, antibodies, and complement proteins circulate in the blood [defense against foreign organisms, toxins]
Protection from blood loss with injuries through clotting mechanisms
Regulation of body temperature, pH, water – maintenance of homeostasis
Interacts with all systems of the body
what regulates heart rate and blood pressure
the nervous system (the medulla in the brain)
where is s2 loudest
at the base of the heart
aortic and pulmonic areas
where is s1 loudest
at the apex of the heart
mitral and tricuspid areas
cardiac output
Amount of blood the heart pumps through the circulatory system in a minute CO = stroke volume X heart rate
stroke volume
Stroke volume = Amount of blood put out by the left ventricle of the heart in one contraction [3-5liters/min]
Dependent on volume of blood in the left ventricle at the end of diastole [LVEDP] = Preload
Dependent on amount of resistance [systemic vascular resistance SVR] heart must overcome to open the aortic valve and push blood out = Afterload
Dependent on Contractility = strength of cardiac muscle to force blood out
Increased preload increases stroke volume
Increased contractility increases stroke volume
Increased afterload [opposes emptying of ventricles] reduces stroke volume
at rest human cardiac output is
approximately 5 litres/minute, rising to 22 litres/minute during maximum physical exertion
cardiac reserve
Increase in CO as related to an increase in HR or SV to meet body requirements
Measures the ability of the heart to increase demand beyond its usual workload
It measures the capacity of the heart to pump blood beyond what is required under normal circumstances of daily life
Dependent on the state of the myocardium and the degree to which the cardiac muscle fibers can be stretched by the volume of blood filling heart during diastole
Maximum increase in CO above the normal value expressed as percentage
The difference between maximum exercise/efficiency and resting CO
Maximum percentage that the CO can increase above normal
Usually 300-400%; 500-600% for athletes
Decreases with heart failure
ejection fraction
Percentage of blood that is pumped out of a filled ventricle with each heartbeat
how to measure ejection fraction
An LV ejection fraction of 50 percent or higher is considered normal.
An LV ejection fraction of less than 50 percent is considered reduced
reduced LV ejection fraction could be caused by
Weakness of heart muscle such as cardiomyopathy
Damaged heart muscle from heart attack
Heart valve problems
Long-term uncontrolled high BP
blood pressure
Strength/force of the blood pushing against the arteries
Systolic = the amount of pressure in the arteries during the contraction of the heart
Diastolic = the pressure in the arteries when the heart relaxes
blood pressure regulated by
Peripheral resistance—when increased impedes blood flow which results in blood backup in the arteries – reduction in diameter of vessel for blood flow vasoconstriction OR increase in blood viscosity
Cardiac output—increased by increase in blood volume
Increase in either will increase BP
mean arterial pressure
Average pressure in a patient’s arteries during one cardiac cycle
Considered a better indicator of perfusion to vital organs than systolic blood pressure (SBP)
Usually determined with invasive monitoring
Can be calculated:
MAP = SBP + 2 (DBP) 3
pressure natriuresis (PN) and BP control
Maintenance of BP at a steady state is influenced by intravascular volume (volume of blood circulating and perfusing body)
Intravascular volume is influenced by vascular tone and extracellular fluid volume (ECFV); ECFV is determined by sodium balance
With BP increase, renal arterial pressure (RAP) increases
Kidney responds by increasing sodium excretion and reducing the ECFV
With BP decrease, renal arterial pressure (RAP) decreases
Kidney responds by decreasing sodium excretion and increasing the ECFV
PN is a renal response to changes in RAP
Steady state BP is the point at which ECFV and PN are in equilibrium
PN = effect of pressure to increase sodium excretion;
Raised BP increases sodium excretion
patho of high and low BP
Significant fluid loss: hemorrhage, diarrhea, vomiting, sweating
Renal disease: sodium and water regulation impacted by malfunctioning kidneys/renal system
Cardiac disease: impairs heart’s ability to pump blood which compromises perfusion of body tissues, and water and sodium balance
Tumours of glands/organs which facilitate maintenance of the water-sodium balance: increase or decrease in hormone production
Rigidity of arterial wall: as in arteriosclerosis
Prolonged standing still: venous pump not efficient with moving blood in lower extremities
hypertensive emergency
Elevated uncontrolled BP results in end-organ damage
CNS, Cardiovascular, renal system
hypertensive urgency
No evidence of end-organ damage
complicated hypertension
Chronic hypertension damages walls of systemic blood vessels hypertrophy and hyperplasia with fibrosis of the tunica intima and media
target organs for hypertension
kidney, brain, heart, extremities and eyes
cardiovascular complications with hypertension
LV hypertrophy Angina pectoris CHF (* left ventricular heart failure) CAD MI Sudden death
vascular complications of hypertension
The formation, dissection and rupture of aneurysms
Intermittent claudication
Gangrene results from vessel occlusion
renal complications of hypertension
Parenchymal damage
Nephrosclerosis
Renal arteriosclerosis
Renal insufficiency or failure microalbuminuria early sign of impending renal dysfunction
retinal complications of hypertension
Vascular sclerosis
Exudation
Hemorrhage
malignant hypertension
Diastolic pressure > 140 mmHg
Linked to dysfunction of renin and angiotensin
Can cause encephalopathy due to high arterial pressure
May also cause papilledema, cardiac failure, uremia, retinopathy and CVA
Considered hypertensive crisis – requiring vasodilators to lower BP
nursing diagnosis for chronic hypertension
Based on Medical diagnosis and assessment of patient illness situation/lived experience
Consider:
Patient teaching on lifestyle changes, diet changes
Monitoring own BP
Awareness of symptoms of progression of illness, stroke, MI
two categories of hypertension in peds
essential hypertension (no identifiable secondary cause) and secondary hypertension (results from an identifiable cause)
hypertension in children and adolescents
SBP or DBP consistently at or over the ninety-fifth percentile
Stage I HTN: BP readings between the ninety fifth and ninety-ninth percentile
Stage II HTN: BP readings over the ninety-ninth percentile plus 5 mmHg
Prehypertension (or high-normal BP): BP 120/80 or greater
secondary hypertension in peds
Occurs secondary to a structural abnormality or underlying pathological process
Most common cause of secondary hypertension is renal disease followed by cardiovascular, endocrine and some neurological disorders
* the younger the child and the more severe the hypertension, the more likely it is to be secondary
essential hypertension in peds
Cause undetermined – linked to genetics, poor diet, lack of exercise, obesity
assessment and diagnosis of hypertension in peds
Routine assessment for healthy children over 3 years old
Should be completed for children less than 3 years old who:
High risk family histories
Risk factors such as CHD, kidney disease, malignancy, transplant, certain neurological problems or systemic illnesses known to cause hypertension
clinical manifestations of hypertension in peds
Adolescents and Older Children: frequent headaches, dizziness, changes in vision
Infants or Young Children: irritability, head banging or head rubbing, waking up screaming in the night
endocrine hypertension
caused by hormonal imbalance Primary Aldosteronism Pheochromocytoma Cushing’s syndrome Hyperparathyroidism Hypo- and Hyperthyroidism
hyperaldosteronism
Common endocrine cause of HTN
Patient presents with HTN and often, hypokalemia (if severe, will include muscle weakness, cramping, headaches, palpitations, polyuria)
causes of hyperaldosteronism
primary adrenal disorder or secondary due to excessive stimulation of the normal adrenal cortex by substances such as angiotensin II, ACTH or elevated potassium
primary hyperaldosteronsim
Primary (Conn’s Syndrome): problem of the adrenal glands releasing too much aldosterone
presents with hypokalemia, weakness, hypertension, renal potassium wasting and neuromuscular manifestations
secondary hyperaldosteronism
results from a problem elsewhere such as heart, liver, kidneys, high blood pressure
presentation due to sustained elevated renin release and activation of angiotensin II
pheochromocytoma
Catecholamine-secreting tumor which causes adrenomedullary hyperfunction
patho of pheochromocytoma
Pathophysiology: Tumors cause adrenal glands to produce too much catecholamines irregularly [epinephrine and norepinephrine]:
Varying frequency and duration
Increase frequency with growth of tumor
4 classic signs and symptoms of pheochromocytoma
headaches, palpitations, diaphoresis, severe hypertension
additional clinical manifestations of pheochromocytoma
Tremor Nausea Weakness Pallor Anxiety, sense of doom Epigastric pain Flank pain Constipation Weight loss
complications of pheochromocytoma
tumors are vascular and can rupture
Patient present with sudden or unexplained decrease in blood pressure, sudden, severe abdominal pain and a rigid abdomen
metabolic syndrome
Clustering of clinical traits that increase risk for cardiovascular disease and type 2 diabetes mellitus
other names for metabolic syndrome
Dysmetabolic syndrome Hypertriglyceridemic waist Insulin resistance syndrome Obesity syndrome Syndrome X
metabolic syndrome traits
Must have 3 of 5 traits:
Increased waist circumference (>40 inches in men; >35 inches in women)
“apple-shaped”
Plasma triglycerides > 1.7 mmol/L
HDL <1.0 mmol/L for men or <1.3 mmol/L for women
BP ≥130/85 mmHg
Fasting Plasma glucose ≥5.6 mmol/L
risk factors for metabolic syndrome
Abdominal obesity Inactive lifestyle Insulin resistance Smoking [as is a risk for heart disease] -Overweight children and adolescents at risk for metabolic syndrome -May develop during childhood
treatment for metabolic syndrome
Heart-healthy lifestyle changes: heart-healthy eating healthy weight managing stress physical activity Quit smoking
atherosclerotic mi’s
Majority of MIs (~90%) caused by thrombus obstructing atherosclerotic coronary artery
Causes acute reduction in blood supply to that part of myocardium
Causes damage to heart muscle
Irreversible death of myocardial cells caused by ischemia
nonatherosclerotic causes of mi’s
Coronary occlusion secondary to vasculitis
Ventricular hypertrophy (eg, left ventricular hypertrophy, hypertrophic cardiomyopathy)
Coronary artery emboli, secondary to cholesterol, air, or the products of sepsis
Coronary trauma
Primary coronary vasospasm (variant angina)
Drug use (eg, cocaine, amphetamines, ephedrine)
Arteritis
Coronary anomalies, including aneurysms of coronary arteries
Factors that increase oxygen requirement, such as heavy exertion, fever, or hyperthyroidism
Factors that decrease oxygen delivery, such as hypoxemia of severe anemia
Aortic dissection, with retrograde involvement of the coronary arteries
Respiratory infections, particularly influenza
coronary atherosclerosis
Abnormal accumulation of lipid, or fatty substances and fibrous tissue in lining of arterial blood vessel walls.
patho of coronary atherosclerosis
Damaged endothelium vulnerable to LDL entrance; Begins as fatty streaks of lipids in arterial walls
LDL embedded in the vessel wall modified with antigenic properties; Attracts leucocytes with Inflammatory effects to infiltrate the injured endothelium
Fibrofatty lesion evolves from streaks; with calcification and continued fibrosis at later stages
Plague growth can restrict lumen and impede perfusion [as in angina and ischemia]
Unstable plaques can rupture and lead to thrombus formation that leads to MI
risk factors for angina
Elevated blood lipids Smoking HTN DM Obesity Family history of premature CV disease Age Metabolic syndrome
LDL cholesterol levels
An LDL cholesterol level of less than 2.6 mmol/L (100 mg/dL) is considered optimal
2.6 to 3.4 (100 to 129) is considered near optimal
3.5 to 4.1 (130 to 159) is considered borderline high
4.2 to 4.9 (160 to 189) is considered high
5.0 and above (190) is considered very high
Specific target LDL depends on type of risk; lower LDL levels recommended for those with higher risks for heart disease
CABG surgery
A saphenous vein from the lower leg or left internal mammary artery (LIMA) is used to bypass the obstructed coronary artery
treatment for heart failure
Angiotensin-converting enzyme inhibitors Angiotensin II receptor blockers Beta-blockers Diuretics Digitalis Other medications
diagnostic criteria for heart failure
Major Criteria (Heart Failure diagnosis requires 2 or more positive) Acute pulmonary edema. Cardiomegaly. Hepatojugular reflex. Neck vein distention. Paroxysmal nocturnal Dyspnea or Orthopnea. Pulmonary rales. Third Heart Sound (S3 Gallup Rhythm)
cardiomyopathy
Diverse group of diseases associated with dysfunction of the myocardium usually with ventricular hypertrophy or dilatation and due to a variety of causes often genetic
inherited or acquired cardiomyopathy
Acquired caused by the effects of neurohormonal responses to ischemic heart disease or hypertension; OR
Secondary to infectious disease, exposure to toxins, systemic connective tissue disease, infiltrative and proliferative disorders, or nutritional deficits; OR
Use of cocaine, amphetamines, anabolic steroids, excessive alcohol
three categories of cardiomyopathy
Dilated cardiomyopathy
Hypertrophic cardiomyopathy
Restrictive cardiomyopathy
dilated cardiomyopathy
Characterized by left ventricular dilation and grossly impaired systolic function leading to dilated heart failure
Most cases are idiopathic but other causes are ischemic heart disease or valvular heart disease, diabetes, renal failure, alcohol use, drug toxicity, nutritional deficiencies post partum, post infectious and hyperthyroidism
Leads to diminished myocardial contractility, diminished ejection fraction, increased end-diastolic and residual volumes
hypertrophic cardiomyopathy
Hypertrophic obstructive cardiomyopathy
Most common of inherited cardiac disorders
Thickening of septal wall which cause outflow obstruction to LV
Occurs when HR is increased and volume is decreased
Diastolic relaxation is impaired
Extra heart sounds or murmurs
Hypertensive or valvular hypertrophic cardiomyopathy
Increased resistance to ventricular ejection seen in hypertension in valvular stenosis (aortic)
Hypertrophy of the myocytes in an attempt to compensate for increased workload
restrictive cardiomyopathy
Characterized by restrictive filling and reduced diastolic volume of either or both the ventricles
May be idiopathic or as a manifestation of scleroderma, amyloidosis, sarcoidosis, lymphoma and hemochromatosis
Myocardium becomes rigid and noncompliant, impeding ventricular filling and raising filling pressures during diastole
Leads to right sided heart failure with systemic venous congestion
Cardiomegaly and dysrhythmias are common
valve dysfunction
Congenital or acquired Acquired due to: Inflammatory Ischemic Traumatic alterations of the valve structure and function Degenerative Infectious
acquired valve dysfunction due to
Rheumatic heart disease (RHD) –most common
Endocarditis
what side heart valves are more commonly affected by dysfunction
left side
structural alterations in valves caused by remodeling of the matrix can lead to
stenosis, incompetence (regurgitation) or both
how to diagnose valve dysfunction
echo
acquired valve dysfunction rheumatic fever
tender and swollen lymph nodes red rash difficulty swallowing thick, bloody discharge from nose temperature of 101°F (38.3°C) or above tonsils that are red and swollen tonsils with white patches or pus small, red spots on the roof of the mouth headache nausea vomiting
acquired valve dysfunction endocarditis
heart murmur pale skin fever or chills night sweats muscle or joint pain nausea or decreased appetite a full feeling in the upper left part of your abdomen unintentional weight loss swollen feet, legs, or abdomen cough or shortness of breath
aortic valve stenosis
Most common
Can be caused by:
congenital bicuspid valve
degeneration with aging
inflammatory damages caused by RHD
Symptoms include:
Breathlessness/Dyspnea
Chest pain (angina), pressure or tightness
Fainting/syncope
Palpitations or a feeling of heavy, pounding, or noticeable heartbeats
Decline in activity level or reduced ability to do normal activities requiring mild exertion
Heart murmur
Weakened carotid pulses
Poor prognosis once patients become symptomatic
mitral valve stenosis
More common in women
Scarring causes leaflets to become fibrous and fused, and chordae tendinae become shortened
Incomplete emptying of the left atrium and elevated atrial pressure atrial dilation and hypertrophy
Increased risk of developing atrial dysrhythmias (What type of dysrhythmia is most common?)
Clinical manifestations are decreased CO, increased pressure in pulmonary circulation—fluid buildup in lungs
Upon auscultation you will hear a murmur
aortic valve regurgitation
Inability of the leaflets to close properly during diastole
Causes may include:
Congenital heart valve disease
Rheumatic fever, bacterial endocarditis, syphilis, HTN, connective tissue disorders, appetite-suppressing medication, trauma or atherosclerosis
Volume overload occurs in the ventricle as blood flows back from aorta and blood filling from atrium – increases preload
SV is increased and CO maintained
Ventricular hypertrophy occurs and eventually leads to heart failure
Clinical manifestations include: widened pulse pressure, turbulence produces a murmur, carotid pulsations and bounding peripheral pulses (Corrigan pulse)
Complications:
Heart failure, infections, dysrhythmias
May use vasodilators and inotropic agents
mitral valve regurgitation
Caused by mitral valve prolapse, RHD, infective endocarditis, MI, connective tissue disease, and dilated cardiomyopathy
Permits back flow from LV into LA producing a murmur
LV becomes dilated and hypertrophied to maintain adequate CO
tricuspid valve regurgitation
More common than stenosis
Associated with failure and dilation of RV secondary to pulmonary HTN
Incompetence leads to volume overload in the RA, increased systemic venous blood pressure, and right sided heart failure
Pulmonic valve dysfunction has the same consequences as tricuspid valve dysfunction
valve repair
Valvuloplasty (repair not replacement) Commissurotomy Repair made to the commissures between the leaflets Annuloplasty Repair made to the annulus of the valve Annuoplasty ring inserted creating an annulus Leaflet Repair Suturing of the leaflets Chordoplasty Repair to the chordae
subjective data of valve dysfunction
May be asymptomatic except heart murmur. If cardiac output is compromised, may see these symptoms: Chest pain Shortness of breath Weakness Fatigue
objective data of valve dysfunction
Heart Murmur
Systolic Murmur – Aortic Stenosis or Mitral Regurgitation
Diastolic Murmur – Aortic Regurgitation or Mitral Stenosis
May be asymptomatic except heart murmur. If cardiac output is compromised, may see these signs:
↓ BP
↑ HR
Skin – cool, diaphoretic, pale, dusky
Weak pulses
Slow cap refill
acute pericarditis
Acute inflammation of the pericardium
pericardial membranes become inflamed and roughened
friction between membranes leads to chest pain
Causes: Infection, autoimmune/inflammatory disorders, uremia, trauma, MI, cancer, radiation therapy, certain drugs
Infectious pericarditis: idiopathic or viral infection
chronic pericarditis
Chronic may be preceded or not by acute pericarditis
Acute phase of any etiology may precede chronic:
Infection (bacterial, viral, fungal, rickettsial or parasitic)
Trauma or surgery
Neoplasm
Metabolic, immunologic or vascular disorder
After major MI
Pericarditis longer than 3 months = Chronic
2 types of Chronic Pericarditis:
Chronic effusive – fluid accumulates in the sac [pericardial effusion]
Chronic constrictive – fibrous tissue forms in pericardium and compresses heart
constrictive pericarditis
Idiopathic or viral infections, radiation therapy for breast cancer or chest lymphoma and heart surgery or any causes of acute pericarditis
Fibrous thickening and calcification of the pericardium causes the visceral and parietal pericardial layers to adhere and become stiff and thickened
Ventricular filling impaired: SV and CO decreased
effusive pericarditis
Idiopathic or cancer, TB, hypothyroidism, CKD
Fluid accumulation in pericardium:
May be serous, serosanguineous, blood, pus, chyle
Purulent pericarditis or hemopericardium may lead to fibrosis of the pericardium
Large effusion leads to cardiac tamponade:
Diastolic filling is impaired leading to decreased CO
Pericardium cannot stretch quickly to accommodate rapid fluid accumulation
patient history and clinical assessment for constrictive pericarditis
Patient history: Dyspnea, fatigue, orthopnea; lower-extremity edema and abdominal swelling; nausea, vomiting and RUQ pain due to hepatic congestion; CP Clinical Assessment: Pulsus paradoxus occasionally Elevated JVP Peripheral edema Hepatomegaly Ascites Cachexia May hear a pericardial knock (early diastolic sound)
patient history and clinical assessment for effusive pericarditis
Patient history: Dyspnea on exertion, fatigue, chest heaviness, peripheral edema Clinical Assessment: Pulsus paradoxus Elevated JVP Tachycardia, tachypnea Decreased/muffled heart sounds Hypotension Peripheral edema Pleural effusion Renal dysfunction
peripheral arterial disease
Atherosclerotic narrowing of the noncardiac, noncranial peripheral arteries
Occurs often in the lower extremities
Modifiable risk factors for PAD are: smoking, obesity, physical inactivity, and a diet high in fats of cholesterol
Non-modifiable risk factors include advanced age and family history, diabetes mellitus, hypertension, hyperlipidemia, and kidney disease (could be modifiable with risk reduction therapies)
Patients are at risk for CV death, stroke, and MI and worse, limb ischemia and lower limb amputation
Often asymptomatic, underdiagnosed, and undertreated
Assessment focuses on finding evidence of atherosclerosis such as auscultation of bruit, absent/diminished pedal pulses, ankle-brachial index, and measuring blood flow using a doppler
Cool skin, abnormal skin color, claudication
peripartum cardiomyopathy (PPCM)
Last month of pregnancy to 5 months post
Difficult to diagnose – HF symptoms similar to third trimester presentation of feet and legs swelling and shortness of breath
Heart chambers enlarge and muscle weakens
Causes decrease in percentage of blood ejected from left ventricle which leads to decrease blood flow and inability of the heart to meet body’s oxygen demands.
Three criteria for diagnosis:
HF develops in last month of pregnancy or within 5 months of delivery
Ejection fraction less that 45%
No other cause for HF
Lab tests to assess:
kidney, liver, thyroid function
Electrolytes including sodium and potassium
CBC
Cardiac injury markers: Troponin, Creatinine Kinase and CK-MB
symptoms of PPCM
Fatigue
Feeling of heart racing or skipping beats (palpitations)
Increased nighttime urination (nocturia)
Shortness of breath with activity and when lying flat
Swelling of the ankles
Swollen neck veins
Low blood pressure, or it may drop when standing up
risk factors for PPCM
Obesity History of cardiac disorders, such as myocarditis (inflammation of the heart muscle) Use of certain medications Smoking Alcoholism Multiple pregnancies African-American descent Poor nourishment
