Heart Failure & Pulmonary HTN Flashcards
Types of HF
- systolic HF
- diastolic HF
- left sided HF
- right sided HF
Systolic HF
- inadequate muscular contraction
- heart dilates
- reduced ejection fraction
- causes: ischemic heart disease, hypertension, idiopathic
- HAVE BIG HEARTS*
Diastolic HF
- inability of heart to relax & allow filling
- normal ejection fraction
- causes: LV hypertrophy, infiltrative disease, myocardial fibrosis
- higher incidence in older patients, diabetics, women
Left sided heart failure
- primarily effects left heart structures
- poor systemic perfusion & increased back PRESSURE ON PULMONARY CIRCUIT
- causes: ischemia, mitral/aortic valve disease, restrictive cardiomyopathies
Right sided heart failure
- 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
Cor Pulmonale: pulmonary hypertensive heart disease
- due pulmonary HTN due to problem w/ lung blood vessels or parenchyma
- results in RV hypertrophy w/ right heart failure
- acute and chronic
Acute cor pulmonale
- pulmonary embolism
- DILATION ONLY
- can cause sudden cardiac death
Chronic cor pulmonale
- RV & atria dilate AND hypertrophy
- in chronic pulmonary HTN the pulmonary arteries develop atheromatous plaques & lesions
Compensatory mechanisms for HF
- frank starling mechanism
- neurohormonal axis: RAAS, SNS
- myocardial structure changes: pressure versus volume overload states
Determinants of ventricular function
- preload
- contractility
- afterload
Determinants of ventricular function: preload
- 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
Determinants of ventricular function: afterload
- 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
Determinants of ventricular function: contractility
- 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
Left sided heart failure symptoms
- dyspnea on exertion (DOE)
- orthopnea
- paroxysmal nocturnal dyspena
- nocturnal cough
- nocturnal awakening
Right sided heart failure symptoms
- abdominal bloating
- hiccups
- anorexia
- weight loss
Left sided heart failure signs
- S3 gallop
- rales
- pleural effusion
- altered respiration
- displaced/diffuse point of maximal impulse (PMI)
Right sided heart failure signs
- elevated JVP
- sternal life
- peripheral edema
- ascites
- hepatomegaly
Volume, pressure, and clinical signs in acute heart failure (wet or dry, warm or cold)
- wet or dry: pulmonary congestion, volume status
- warm or cold: blood pressure, tissue perfusion
Myocardial structural changes
- myocytes can undergo hyperplasia so they undergo hypertrophy
Myocardial structural changes in pressure overload states (HTN/valvular stenosis)
- new sarcomeres added in parallel causing increase muscle fiber diameter
- concentric hypertrophy: THICKER WALL BY NO CHANGE IN CHAMBER SIZE
Myocardial structural changes in volume overload states (valvular regurgitation/shunts)
- 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
Heart failure: microscopic pathology
- myocyte hypertrophy: enlarged cytoplasm & nuclei
- interstitial fibrosis: pericellular and perivascular
LV heart failure effect on other organs
- lungs: infiltrate (fluid build up in alveoli w/ macrophages)
- liver: infiltrative
Staging of heart failure
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***
NYHA functional classification of HF
I: no limitation
II: mild symptoms, slight limitation w/ activity
III: marked symptoms & limitations w/ activity
IV: symptoms at rest
Pharmacologic therapy: systolic heart failure
- ACEIs, ARBs, B-blockers, aldosterone antagonists, diuretics, digoxin, arterial vasodilators/nitrates, inotropes
Pharmacologic therapy: diastolic heart failure
- diuretics
- treat underlying problem: HTN, ischemia, DM
ACEIs effects & when/why
- reduced afterload/preload, reduced aldosterone, inhibition of cardiac and vascular remodeling
- when/why: high risk & LVEF
Contraindications to ACEIs
- pregnancy
- Cr>3.0
- renal stenosis
- hyperkalemia
ARBs
- alternative to ACEIs
- angiotensin II forms and breaks down bradykinin then blocked at receptor
- cough less common b/c bradykinin broken down
B blockers: effects & when/why/how
- effects: block SNS response, reverse cardiac remodeling, improve EF
- when/why/how: post MI, LVEF
B blockers: caution & avoidance
- caution: diabetes w/ recurrent hypoglycemia, HR
Aldosterone antagonists: how & why
- 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
Aldosterone antagonists: side effects & contraindications
- 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
Afterload reduction in those intolerant of ACEIs/ARBs
- 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
Diuretic therapy
- 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
Diuretic risks
- hypokalemia: arrhythmia, muscle aches
- bicarbonate reabsorption–metabolic alkalosis
- decreased uric acid excretion–GOUT
- hyponatremia
- further neurohormonal activation STOP WHEN POSSIBLE
Digitalis glycosides: mechanism
- positive inotropic effect by increasing Ca & enhancing actin-myosin cross bridge formation
- vagotonic effect
- arrhythmogenic effects
Digitalis glycosides: role
- role declined recently due to safety concern
- does not effect mortality of CHF patients but causes significant reduction in hospitalization & symptoms
Digitalis toxicity
- NARROW THERAPEUTIC TO TOXIC RATIO
- non cardiac manifestations: anorexia, nausea, vomiting, headache, visual changes, disorientation
- cardiac manifestations: sinus bradycardia, AV block, atrial tachycardia
Cardiac Inotropes
- 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
Benefits & Negative Side effects of inotropes
- benefits: increased contractility, CO, decreased PVR
- adverse: increased myocardial O2 consumption, hypotension, tachycardia, arrhythmias, worsening HF, CAN SHORTEN SURVIVAL
Most common presentation of heart failure
- warm & wet
- No hypoperfusion, congested
Warm & wet treatment
- diuretics, vasodilators
Cold and wet treatment
- diuretics
- vasodilators
- inotropes
Cold and dry treatment
- fluids
- inotropes
Non pharmacologic therapy
- patient education
- home monitoring
- symptom management
- dietary, lifestyle, exercise
Impact of heart failure (HF) statistics
- 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
