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MOHDIII - Unit 2 > Heart Failure & Pulmonary HTN > Flashcards

Heart Failure & Pulmonary HTN Flashcards

1
Q

Types of HF

A
  • systolic HF
  • diastolic HF
  • left sided HF
  • right sided HF
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2
Q

Systolic HF

A
  • inadequate muscular contraction
  • heart dilates
  • reduced ejection fraction
  • causes: ischemic heart disease, hypertension, idiopathic
  • HAVE BIG HEARTS*
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3
Q

Diastolic HF

A
  • inability of heart to relax & allow filling
  • normal ejection fraction
  • causes: LV hypertrophy, infiltrative disease, myocardial fibrosis
  • higher incidence in older patients, diabetics, women
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4
Q

Left sided heart failure

A
  • primarily effects left heart structures
  • poor systemic perfusion & increased back PRESSURE ON PULMONARY CIRCUIT
  • causes: ischemia, mitral/aortic valve disease, restrictive cardiomyopathies
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5
Q

Right sided heart failure

A
  • MOST COMMON CAUSE IS LEFT HEART FAILURE
  • isolated RV failure related to severe pulmonary HTN, congenital heart disease w/ left to right shunts & tricuspid/pulmonic valve disorders
  • effects due to back on systemic and portal venous systems
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6
Q

Cor Pulmonale: pulmonary hypertensive heart disease

A
  • due pulmonary HTN due to problem w/ lung blood vessels or parenchyma
  • results in RV hypertrophy w/ right heart failure
  • acute and chronic
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7
Q

Acute cor pulmonale

A
  • pulmonary embolism
  • DILATION ONLY
  • can cause sudden cardiac death
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8
Q

Chronic cor pulmonale

A
  • RV & atria dilate AND hypertrophy

- in chronic pulmonary HTN the pulmonary arteries develop atheromatous plaques & lesions

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9
Q

Compensatory mechanisms for HF

A
  • frank starling mechanism
  • neurohormonal axis: RAAS, SNS
  • myocardial structure changes: pressure versus volume overload states
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10
Q

Determinants of ventricular function

A
  • preload
  • contractility
  • afterload
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11
Q

Determinants of ventricular function: preload

A
  • amount of stretch on ventricle at end of diastole
  • reflects ventricular pressure & volume
  • estimated by end diastolic pressure (EDP)
  • frank starling: increased EDP causes more stretch causing stronger contraction and increased CO
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12
Q

Determinants of ventricular function: afterload

A
  • load against which heart must eject blood
  • reflects compliance of large arteries (aorta for LV & pulmonary arteries for RV) and the resistance in the small vessels
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13
Q

Determinants of ventricular function: contractility

A
  • intrinsic ability of heart muscle to contract
  • INDEPENDENT of preload and afterload
  • changes in myosin binding can increase or decrease force
  • can’t measure clinically
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14
Q

Left sided heart failure symptoms

A
  • dyspnea on exertion (DOE)
  • orthopnea
  • paroxysmal nocturnal dyspena
  • nocturnal cough
  • nocturnal awakening
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15
Q

Right sided heart failure symptoms

A
  • abdominal bloating
  • hiccups
  • anorexia
  • weight loss
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16
Q

Left sided heart failure signs

A
  • S3 gallop
  • rales
  • pleural effusion
  • altered respiration
  • displaced/diffuse point of maximal impulse (PMI)
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17
Q

Right sided heart failure signs

A
  • elevated JVP
  • sternal life
  • peripheral edema
  • ascites
  • hepatomegaly
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18
Q

Volume, pressure, and clinical signs in acute heart failure (wet or dry, warm or cold)

A
  • wet or dry: pulmonary congestion, volume status

- warm or cold: blood pressure, tissue perfusion

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19
Q

Myocardial structural changes

A
  • myocytes can undergo hyperplasia so they undergo hypertrophy
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20
Q

Myocardial structural changes in pressure overload states (HTN/valvular stenosis)

A
  • new sarcomeres added in parallel causing increase muscle fiber diameter
  • concentric hypertrophy: THICKER WALL BY NO CHANGE IN CHAMBER SIZE
21
Q

Myocardial structural changes in volume overload states (valvular regurgitation/shunts)

A
  • new muscle fibers added in series thus muscle fiber length increases
  • leads to VENTRICULAR DILATION, wall thickness can change or not
  • hypertrophy measure in weight NOT thickness
22
Q

Heart failure: microscopic pathology

A
  • myocyte hypertrophy: enlarged cytoplasm & nuclei

- interstitial fibrosis: pericellular and perivascular

23
Q

LV heart failure effect on other organs

A
  • lungs: infiltrate (fluid build up in alveoli w/ macrophages)
  • liver: infiltrative
24
Q

Staging of heart failure

A 
A: high risk for developing
B: Asymptomatic HF
C: Symptomatic HF
D: End stage HF
***one way street, patients move from A to D but NEVER backwards***
25
Q

NYHA functional classification of HF

A

I: no limitation
II: mild symptoms, slight limitation w/ activity
III: marked symptoms & limitations w/ activity
IV: symptoms at rest

26
Q

Pharmacologic therapy: systolic heart failure

A
  • ACEIs, ARBs, B-blockers, aldosterone antagonists, diuretics, digoxin, arterial vasodilators/nitrates, inotropes
27
Q

Pharmacologic therapy: diastolic heart failure

A
  • diuretics

- treat underlying problem: HTN, ischemia, DM

28
Q

ACEIs effects & when/why

A
  • reduced afterload/preload, reduced aldosterone, inhibition of cardiac and vascular remodeling
  • when/why: high risk & LVEF
29
Q

Contraindications to ACEIs

A
  • pregnancy
  • Cr>3.0
  • renal stenosis
  • hyperkalemia
30
Q

ARBs

A
  • alternative to ACEIs
  • angiotensin II forms and breaks down bradykinin then blocked at receptor
  • cough less common b/c bradykinin broken down
31
Q

B blockers: effects & when/why/how

A
  • effects: block SNS response, reverse cardiac remodeling, improve EF
  • when/why/how: post MI, LVEF
32
Q

B blockers: caution & avoidance

A
  • caution: diabetes w/ recurrent hypoglycemia, HR
33
Q

Aldosterone antagonists: how & why

A
  • how: K+ sparing diuretic, aldosterone inhibition minimize K+ loss, prevent sodium & water retention, endothelial dysfunction and myocardial fibrosis
  • why: spironolactone can be adde to loop diuretics to enhance diuresis
34
Q

Aldosterone antagonists: side effects & contraindications

A
  • side effects: hyperkalemia, impotence/menstrual changes, gynecomastia (eplerenone more aldosterone selective)
  • contraindicated: Cr>2.5 (or >2 for women), K+>5
  • *check K+ and renal function at 3 days or week, monthly x3 and q3mo
35
Q

Afterload reduction in those intolerant of ACEIs/ARBs

A
  • direct arterial vasodilators: hydralazine-decrease PVR, combine w/ nitrates, can add background therapy if remain hypertensive
  • nitrates: combined venodilator/arterial vasodilator, need nitrate free period to avoid intolerance, good choice in patients w/ ANGINA
36
Q

Diuretic therapy

A
  • most effective symptomatic relief
  • LOOP DIURETICS are most used in heart failure
  • mechanism: inhibit chloride reabsorption in ASCENDING LOOP OF HENLE results in natriuresis, kaliuresis and metabolic alkalosis
  • thiazide diuretics often combined w/ loop diuretics
37
Q

Diuretic risks

A
  • hypokalemia: arrhythmia, muscle aches
  • bicarbonate reabsorption–metabolic alkalosis
  • decreased uric acid excretion–GOUT
  • hyponatremia
  • further neurohormonal activation STOP WHEN POSSIBLE
38
Q

Digitalis glycosides: mechanism

A
  • positive inotropic effect by increasing Ca & enhancing actin-myosin cross bridge formation
  • vagotonic effect
  • arrhythmogenic effects
39
Q

Digitalis glycosides: role

A
  • role declined recently due to safety concern

- does not effect mortality of CHF patients but causes significant reduction in hospitalization & symptoms

40
Q

Digitalis toxicity

A
  • NARROW THERAPEUTIC TO TOXIC RATIO
  • non cardiac manifestations: anorexia, nausea, vomiting, headache, visual changes, disorientation
  • cardiac manifestations: sinus bradycardia, AV block, atrial tachycardia
41
Q

Cardiac Inotropes

A
  • Phosphodiesterase III Inhibitors (MILRINONE): positive inotrope, arterial/venous vasodilator, “ino-dilator”
  • Beta adrenergic stimulation agent (DOBUTAMINE): stimulates B1>B2>alpha receptors, strong inotrope w/ weak vasodilatory effect due to B2 stimulation, tolerance may develop
42
Q

Benefits & Negative Side effects of inotropes

A
  • benefits: increased contractility, CO, decreased PVR
  • adverse: increased myocardial O2 consumption, hypotension, tachycardia, arrhythmias, worsening HF, CAN SHORTEN SURVIVAL
43
Q

Most common presentation of heart failure

A
  • warm & wet

- No hypoperfusion, congested

44
Q

Warm & wet treatment

A
  • diuretics, vasodilators
45
Q

Cold and wet treatment

A
  • diuretics
  • vasodilators
  • inotropes
46
Q

Cold and dry treatment

A
  • fluids

- inotropes

47
Q

Non pharmacologic therapy

A
  • patient education
  • home monitoring
  • symptom management
  • dietary, lifestyle, exercise
48
Q

Impact of heart failure (HF) statistics

A
  • 6+ million americans
  • nearly 700,000 new cases/year
  • more than 280,000 die of HF/year in US: 2nd highest mortality at 1 yr
  • 1/9 death certificates mentioned HF in 2008
  • 20% die in first yr of diagnosis, 50%by 5 yrs, 80% by 10 yrs

MOHDIII - Unit 2 (23 decks)

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