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Cardiopulmonary Renal > Hypertension And Heart Failure > Flashcards

Hypertension And Heart Failure Flashcards

1
Q

What is the definition of hypertension ?

A

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

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2
Q

What is a hypertensive crisis ?

A

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

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3
Q

What are the risk factors for hypertension?

A

Age, obesity, diabetes, physical inactivity, excess salt intake, excess alcohol intake, family history; African American > Caucasian > Asian

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4
Q

What are the classifications of hypertension?

A

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

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5
Q

What are the causes of secondary hypertension?

A

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

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6
Q

What is ump based- hypertension?

A

increased CO

Occurs In younger patients, amenable to beta blockers * (overdeveloped alerting response; excessive sympathetic effects on heart).

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7
Q

Whaat are vascular resistance-based hypertension ?

A

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)

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8
Q

What is Volume-based hypertension?

A

Increased retention of Na and H2O

Renal parenchyma disease, renovascular disorders. (Failure of the Renin Angiotendin System to regulate BP)

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9
Q

Explain the neurogenic or stress hypothesis

A
  1. 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

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10
Q

What the positive feedback of neurogenic /stress hypothesis ?

A

Vascular hypertrophy—> narrowed arteries—> increased blood pressure —> vascular hypertrophy

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11
Q

Summarize neurogenic /stress hypertension

A

Sustained pump activity + sustained vascular resistance= sustained blood pressure (neurogenic or stress)

  • leads to vascular hypertrophy
  • leads vasoconstriction
  • further narrow arteries
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12
Q

Outline salt imbalance or renal hypothesis (volume based) hypertrophy

A

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

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13
Q

Explain baroreceptor compensation

A

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

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14
Q

Explain renin angiotensin system compensation

A

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

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15
Q

What are the main receptors of baroreceptor reflex?

A
  • 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)
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16
Q

What are the baroreceptors of the baroreceptor reflex arch

A
  • 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
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17
Q

What are the chemoreceptors of the baroreceptor reflex?

A
  • 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
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18
Q

What are possible non drug therapy to treat hypertension ?

A
  • reduce BMI
  • regular physical exercise
  • increased consumption of fruits and vegetables
  • restricts salt intake
  • quit smoking
  • low saturated fat diet
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19
Q

What are the drug therapies to treat hypertension ?

A

a1 receptor antagonists

Angiotensin converting enzyme inhibitors

Angiotensin II receptor blockers

B adrenergic blockers

Calcium channel

Thiazide and thiazides like diuretics

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20
Q

How do a1 receptor antagonists treat hypertension?

A

Decreased TPR

21
Q

How does angiotensin converting enzyme inhibitor prevent hypertension?

A

Decreased Angiotensin II and aldosterone

Decreased vascular tone and decreased ECF volume

22
Q

How do angiotensin II receptor blockers treat hypertension?

A

Decreased vascular tone and decreased ECF volume

23
Q

How do B blockers treat hypertension ?

A

Reduced Contractility, reduced rate- decreased CO

24
Q

How do calcium channel blockers treat hypertension ?

A

Decreased TPR

25
Q

How does thiazide and thiazide like diuretics treat hypertension ?

A

Decreased ECF

26
Q

What are the consequences of hypertension being left untreated?

A
  • 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)

27
Q

What is congestive cardiac failure?

A

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

28
Q

What are the clinical features of congestive cardiac failure?

A

Exercise intolerance

Breathlessness (dyspnea)

Fatigue

Peripheral edema

29
Q

What is the prevalence of congestive cardiac failure ?

A

1%. At age 50 and 9% at age 80

400,000 new cases each year in the US

30
Q

What is the mortality of congestive heart failure?

A

50% die within 5 years of diagnosis (untreated). Death is due to pump failure or arrythmias

Most common diagnosis of hospitalized patients > 65 years

31
Q

What are the predisposing conditions ti cingestive heart failure?

A

Chronic hypertension

Coronary artery disease

Valvular heart disease

32
Q

Explain classifications of congestive heart failure

A

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

33
Q

How can heart failure be classified in relation to other diseases?

A

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

34
Q

How do we know the heart is failing?

A

Stroke volume

Heart rate

35
Q

How can stroke volume indicate heart failure?

A

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%)

36
Q

How does contractility lead to heart failure?

A

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

37
Q

How does afterload lead to congestive cardiac failure?

A

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

38
Q

How does diastolic function lead to cardiac failure?

A

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

39
Q

What systolic features of cardiac failure?

A

Reduced contractility

Reduced stroke volume

Frank sterling curvevshifts

More common than diastolic failure

Both can be present

40
Q

What are the diastolic features of heart failure?

A
  • failing in filling (mitral stenosis )
  • Reduced end diastolic volume
  • Reduced stroke volume
41
Q

Can there be overlap of systolic and diastolic heart failure features?

A

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

42
Q

Describe the pressure volume loop with someone with systolic heart failure

A

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

43
Q

Describe the pressure volume loop in someone with diastolic heart failure

A

(PRESERVED EF)

Decreased ventricular compliance with yypertrophy

Leads to:

  • increased end diastolic pressure
  • reduced ventricle filling
  • near normal EF
  • reduced SV
44
Q

What are some clinical consequences of decreased

A

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

45
Q

What are the consequences of edema?

A

RV edema—> peripheral edema—> ankle swelling—> pitting edema

LV edema—> pulmonary edema—> breathlessness(dyspnea)—> worse when supine (orthopnea)

46
Q

Summarize consequences of LV failure on the RV (and vice versa)

A

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)

47
Q

Explain the compensatory mechanism of chronic cardiac failure

A

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
48
Q

How can continued activation of compensatory mechanisms become ultimately harmful?

A

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

Cardiopulmonary Renal (35 decks)

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