Hypertension And Heart Failure Flashcards
What is the definition of hypertension ?
Normal: less than 120/80mmHg;
Elevated: systolic between 120-129 and diastolic less than 80;
Stage 1: systolic between 130-139 or diastolic between 80-89
Stage 2: systolic at least 140 or diastolic at least 90 mmHg
What is a hypertensive crisis ?
Systolic above 180 and/ or diastolic above 120, with patients needing prompt changes in medication if there are no other indications of problems, or immediate hospitalization if there are signs of organ damage
What are the risk factors for hypertension?
Age, obesity, diabetes, physical inactivity, excess salt intake, excess alcohol intake, family history; African American > Caucasian > Asian
What are the classifications of hypertension?
Hypertension —> primary (essential )
Primary- benign (most common, slow progression)
Primary- malignant(rare, rapid progression, medical emergency)
Only 10% of cases- specific disease or abnormality- secondary
What are the causes of secondary hypertension?
Renal artery stenosis- MAP in afferent arteriole is decreased > activation of RAS> increased Angiotensin II
Renal disease- decreased ability to excrete Na+ and water (increased blood volume)
Conn’s syndrome (hyper aldosteronism): increased salt and retention
Pheochromocytoma: increased secretion of epinelhrine
Pre-enclampsia toxemia: increased blood pressure of pregnancy
Hyperthyroidism: increased systolic blood pressure by decreasing systemic vascular resistance, increasing heart rate, and raising cardiac output
Cushings disease/syndrome - overexpression of renin-angiotensin system
What is ump based- hypertension?
increased CO
Occurs In younger patients, amenable to beta blockers * (overdeveloped alerting response; excessive sympathetic effects on heart).
Whaat are vascular resistance-based hypertension ?
Increased TPR
Occurs more in older patients. (Smooth muscle abnormally sensitive to vasoconstrictors, endothelial cell dysfunction- abnormal regulation of vascular tone by local factors e.g. NO)
What is Volume-based hypertension?
Increased retention of Na and H2O
Renal parenchyma disease, renovascular disorders. (Failure of the Renin Angiotendin System to regulate BP)
Explain the neurogenic or stress hypothesis
- Exaggerated alerting responses—> increased sympathetic outflow—> bouts of reversible hypertension—> vascular smooth muscle hypertrophy —> vasoconstriction—> chronic increased TPR
Other pathological factors:
-loss of elastin —> arteriosclerosis changes in arteries—> large increase in systolic BO
What the positive feedback of neurogenic /stress hypothesis ?
Vascular hypertrophy—> narrowed arteries—> increased blood pressure —> vascular hypertrophy
Summarize neurogenic /stress hypertension
Sustained pump activity + sustained vascular resistance= sustained blood pressure (neurogenic or stress)
- leads to vascular hypertrophy
- leads vasoconstriction
- further narrow arteries
Outline salt imbalance or renal hypothesis (volume based) hypertrophy
Discrepancy between Na+ intake and Na+ excretion —> increased ECF —> increased plasma—> increased CVP —>. Increased venous return —> increased SV & BP —> vascular smooth hypertrophy —> vasoconstriction—> increased TPR
Explain baroreceptor compensation
Baroreceptors modulate moment to moment changes in BP- not involved in long term regulation
Baroreceptor reflex doesn’t prevent development of chronic HTN because baroreceptors constantly reset themselves
Carotid sinus baroreceptor nerve firing rate and mean arterial pressure
About 1-2 days of high BP- baroreceptor furing (initially increased) goes back to normal (rapidly adapting receptors!) note: the baroreceptor reflex still operated in hypertension, but it operates around an elevated set point
Explain renin angiotensin system compensation
Increased renal artery pressure leads to increased GFR and increased excretion of Na+ and H2O
But in HTN, the pressure-naturesis curve is shifted to the right, shift of curve could be due to renal tissue damage or renin angiotensin system (RAS)
In HTN, higher arterial pressure required to excrete Na+ and H2O; retention resultin in increased blood volume
However, sustained increase in blood volume= increased sustained blood pressure
What are the main receptors of baroreceptor reflex?
- Aortic arch transmits via vagus nerve to solitary nucleus of medulla (responds to changes in BP )
- Carotid sinus (dilated region at carotid bifurcation) transmits via glossopharyngeal nerve to solitary nucleus of medulla (upwards)
What are the baroreceptors of the baroreceptor reflex arch
- Hypotension - decreased arterial pressure —> decreased stretch —> decreased Afferent baroreceptor —> increased sympathetic firing and decreased efferent parasympathetic stimulation—> vasoconstriction, increased heart rate, increased contractility, increased BP. Important in the response to severe hemorrhage
- Carotid massage— increased pressure on carotid sinus —> increased stretch—> increased Afferent baroreceptor firing —> increased AV node refractory period —> increased HR
- Component of Cushing reflex (triad of hypertension, bradychardia, and respiratory depression)— increased intracranial pressure constricts arterioles —> cerebral ischemia —> PCO2 and decreased pH —> central reflex sympathetic increase in perfusion pressure (hypertension) —> increased stretch—> peripheral reflex baroreceptor-induced bradychardia
What are the chemoreceptors of the baroreceptor reflex?
- Peripheral-carotid and aortic bodies are stimulated by increased PCO2, decreased pH of blood, and decreased PO2 (decreased 60 mmHg)
- Central - are stimulated by changes in pH and PCO2 of brain interstitial fluid, which in turn are influenced by arterial CO2 as H+ cannot cross the blood-barrier. Do not directly respond to PO2. Central chemoreceptors become less responsive with chronically increased PCO2 (e.g. COPD)—> increased dependence on peripheral chemoreceptors to detect decreased O2 to drive respiration
What are possible non drug therapy to treat hypertension ?
- reduce BMI
- regular physical exercise
- increased consumption of fruits and vegetables
- restricts salt intake
- quit smoking
- low saturated fat diet
What are the drug therapies to treat hypertension ?
a1 receptor antagonists
Angiotensin converting enzyme inhibitors
Angiotensin II receptor blockers
B adrenergic blockers
Calcium channel
Thiazide and thiazides like diuretics
How do a1 receptor antagonists treat hypertension?
Decreased TPR
How does angiotensin converting enzyme inhibitor prevent hypertension?
Decreased Angiotensin II and aldosterone
Decreased vascular tone and decreased ECF volume
How do angiotensin II receptor blockers treat hypertension?
Decreased vascular tone and decreased ECF volume
How do B blockers treat hypertension ?
Reduced Contractility, reduced rate- decreased CO
How do calcium channel blockers treat hypertension ?
Decreased TPR
How does thiazide and thiazide like diuretics treat hypertension ?
Decreased ECF
What are the consequences of hypertension being left untreated?
- increased work load of LV leading to congestive cardiac failure
- increased risk of vascular disorders leading to cerebral hemorrhage and aortic aneurysms
- deposition of proteins—> loss of nephrons leading to renal damage and chronic renal failure
- increased risk of developing artheroma leading to coronary artery disease
(60% of CVAs and 50% of ischemic heart disease is due to inadequately treated hypertension)
What is congestive cardiac failure?
A pathophysiological state in which an abnormality of cardiac function is responsible for the failure of the heart to pump blood at a rate commensurate with the requirements of the metabolizing tissue
What are the clinical features of congestive cardiac failure?
Exercise intolerance
Breathlessness (dyspnea)
Fatigue
Peripheral edema
What is the prevalence of congestive cardiac failure ?
1%. At age 50 and 9% at age 80
400,000 new cases each year in the US
What is the mortality of congestive heart failure?
50% die within 5 years of diagnosis (untreated). Death is due to pump failure or arrythmias
Most common diagnosis of hospitalized patients > 65 years
What are the predisposing conditions ti cingestive heart failure?
Chronic hypertension
Coronary artery disease
Valvular heart disease
Explain classifications of congestive heart failure
New York heart association classifies based if symptom severity and amount to provoke symptoms
Class 1: no limitation of physical activity
Class 2: Slight limitation of physical activity in which ordinary physical activity leads to fatigue, palpitation, dyspnea, or anginal pain; the person is comfortable at rest
Class 3: Marked limitation of physical activity in which less than ordinary activity results in fatigue, palpitation, dyspnea, or anginal pain; the person is comfortable at rest
Class 4: inability to carry on any physical activity without discomfort but also symptoms of heart failure or the anginal syndrome even at rest, with increased discomfort if any physical activity is undertaken
How can heart failure be classified in relation to other diseases?
Heart failure may be the final and most severe manifestation of nearly every form of cardiac disease
Anatomical- left, right and I ventricular
Left- reduced left ventricular output and or increased left atrial or pulmonary venous pressure- mitral stenosis leading to pulmonary congestion
Right- reduced right ventricular output for any given right atrial pressure- failure of both ventricles either due to ischemia or progression of disease
Biventricular- failure of both ventricles either due to ischemia or progression of disease
Function- diastolic and systolic
Systolic- impaired myocardial contraction
Diastolic- poor ventricular filling or abnormal ventricular relaxation
Timeline-Acute and chromic
Acute- sudden e.g. MI
Chronic- gradual impairment, progressive e,g. Valvular heart disease
How do we know the heart is failing?
Stroke volume
Heart rate
How can stroke volume indicate heart failure?
Contractility (decreased calcium uptake in the SR, low affinity of troponin fir calcium, altered substrate metabolism from fatty acid to glucose oxidation, impaired energy production)
Preload events (volume and pressure of blood in ventricles at end diastole)
Afterload events (volume and pressure of blood in the ventricles during systole, resistance to blood leaving the heart)
A good indicator of contractility is the ejection fraction (EF)= the fraction of blood ejected by the ventricle relative to its end-diastolic volume
EF= (SV/EDV) x 100(normal values: 50%-75%)
How does contractility lead to heart failure?
Decreased contractility- impaired systolic function
E.g. ischemic damage, chronic pressure overload, chronic volume overload, non-ischemic dilated cardiomyopathy, infectious diseases, drug induced
Decreased stroke volume, leading to reduced EF( systolic function) —> heart failure
How does afterload lead to congestive cardiac failure?
Increased afterload, impaired systolic function- systemic demands, volume and pressure overload, advanced aortic stenosis, uncontrolled sever hypertension
SV low, EDV is Normal, EF is low
This reduces EF/ Systolic dysfunction- -> heart failure
How does diastolic function lead to cardiac failure?
Impaired diastolic function (restricted filling, increased stiffness) decreased preload
e,g. Pathological myocardial hypertrophy- HPT, ageing, restrictive cardiomyopathy, sarcoidosis, amyloidosis
Decreased EDV EF is within normal range SV is low but EDV is also low
Leads to preserved ejection fraction (diastolic dysfunction)
Leads to heart failure
What systolic features of cardiac failure?
Reduced contractility
Reduced stroke volume
Frank sterling curvevshifts
More common than diastolic failure
Both can be present
What are the diastolic features of heart failure?
- failing in filling (mitral stenosis )
- Reduced end diastolic volume
- Reduced stroke volume
Can there be overlap of systolic and diastolic heart failure features?
There is much overlap, and many outpatients demonstrate both types of features
Current classification: heart failure with reduced ejection fraction : mostly systolic
Heart failure with preserved ejection fraction.: mostly diastolic
Describe the pressure volume loop with someone with systolic heart failure
Decreased EF
Impaired contractility —> increased EDV abd passive with wall stretch decrease leads to:
- increased EDV - increased compliance
- reduced EF
- Increased blood volume (RAS)
- Increased wall stress
Increase work for heart
Describe the pressure volume loop in someone with diastolic heart failure
(PRESERVED EF)
Decreased ventricular compliance with yypertrophy
Leads to:
- increased end diastolic pressure
- reduced ventricle filling
- near normal EF
- reduced SV
What are some clinical consequences of decreased
Decreased contractility- > decreased SV—> decreased ejection fraction—> increased EDV (causes two things, first dilation of heart, then decreased pumping heart)
Second, increased venous pressure, increased capillary hydrostatic pressure, causing edema
What are the consequences of edema?
RV edema—> peripheral edema—> ankle swelling—> pitting edema
LV edema—> pulmonary edema—> breathlessness(dyspnea)—> worse when supine (orthopnea)
Summarize consequences of LV failure on the RV (and vice versa)
LV starts to fail (RV still normal) —> increases LA pressure—> increases pulmonary venous pressure(causing pulmonary edema) —> increases pulmonary artery BP—> increases afterload on RV —> RV starts to fail (causing peripheral edema)
Explain the compensatory mechanism of chronic cardiac failure
Increased TPR, increased blood volume
- Primary abnormality of heart failure is impairment of ventricular function resulting in reduced cardiac output
- Counter-regulatory neurohormonal mechanisms are activated to increase afterload and increase preload
- Mechanisms try to buffer thr fall in CONand help preserve sufficient BP to perfume vital organs
- Renin angiotensin aldosterone system leads to vasoconstriction, NaCl and H2O retention and sympathetic mediation because of angiotensin II( vasoconstrictor)
- Aldisterone enhances salt and water retention
- Endothelin enhances vasoconstriction especially renal vasculature
- ANP- released from atria in response to stretch
- Sympathetic increase myocardial contractility, heart rate and peripheral vasoconstriction
- Prolonged sympathetic lead to hypertrophy and apoptosis
- Ventricular hypertrophy is from increased wall tension
- Hypertrophied ventricles are less compliant: EDP is increased which leads to increased atrial pressure and increased venous pressure
How can continued activation of compensatory mechanisms become ultimately harmful?
Increased blood volume- causes pulmonary edema
Increased TPR - increased afterload, decreased SV & CO
Increased HR- increases metabolic demand
Continuous sympathetic activity- down regulation of B receptors
Increased angiotensin II - increased cytokines abd fibroblasts - adverse remodeling of the heart
Heart now goes in to decompensated state
