Heart Failure & Cor Pulmonale & A-fib/flutter Flashcards
_____ x ______ = cardiac output
stroke volume x heart rate = CO (amount of blood your heart can beat in 1 min (mL/min)
What is stroke volume determined by
preload, afterload, and ventricular contractility (SV = EDV-ESV)
Describe the Frank-Starling law
- greater EDV increases contractile strength of the ventricles which increases SV
- myocardium will be more stretched d/t greater volume which leads to stronger contraction
How does the sympathetic nervous system maintain cardiac output
improves ventricular contractility and HR, systemic arteriolar vasoconstriction
how does the RAAS system maintain cardiac output
- increased angiotensin II, vasoconstrictor that attempts to maintain an adequate BP
- increased aldosterone, hormone that increases plasma volume to maintain adequate ventricular filling (preload)
how does ADH secretion maintain cardiac output
increases ventricular filling (preload) by decreasing water excretion in the urine & increasing thirst
What is the downside of the SNS, RAAS, and ADH secretion maintaining cardiac output in the context of heart failure long term?
structural changes to the heart that are damaging
When is natriuretic peptide released and what can it tell us in the workup for HF (BNP & NT-proBNP labs)
- released d/t stretching of ventricular walls or increased pressure upon the walls
- in HF this increases water and sodium excretion in the urine
- serial BNP levels to guide management of acute HF not established & should not be used in isolation to exclude or confirm HF (high negative predictive value)
Describe the etiology of heart failure
heart unable to pump enough blood to meet body’s need for O2
What is the most common cause of left sided heart failure
CAD (then dilated CMO, restrictive CMO, & hypertrophic CMO)
What is the most common cause of R sided HF
L sided HF
Describe the major types of HF
- HFrEF: EF <40%
- HFpEF: EF >50%
- HFimpEF: EF previously <40% but now greater
- HFmrEF: EF 41-49%
- high output HF
What are the major RFs for HF
CAD, HTN, DM, valvular disease, smoking, obesity
Describe the major signs/symptoms of HF
Fatigue, weakness, dyspnea on exertion, cough, orthopnea, paroxysmal nocturnal dyspnea, GI sxs, weight gain, LE edema
Labored breathing, need to sit upright, sinus tach (increased adrenergic activity), peripheral vasoconstriction (cool extremities, cyanosis of lips & nail beds)
Describe the diagnostic testing for HF
EKG: may see acute ischemia as cause of new-onset HF, may provide info about etiology of HF (arrhythmia, LVH), low specificity
Labs: CBC, CMP (renal fx, electrolytes - Na & K, liver enzymes), cardiac enzymes, brain or B-type natriuretic peptide (BNP) and N-terminal BNP (NT-proBNP)
CXR: helpful in identifying cardiac v pulmonary etiology, signs of acute decompensated HF include cardiomegaly, pleural effusion, interstitial edema (Kerley B lines), cephalization of vessels (upper lobe vessels larger than lower lobe vessels)
Echo: assess size & function of chambers, valves, pericardial effusion, shunting & regional wall motion, segmental wall abnormalities, determines LV EF
Describe the etiology/causes of cor pulmonale
Pulmonary HTN induced altered structure (hypertrophy or dilation) and/or impaired fx of R ventricle associated with chronic lung disease/hypoxemia
Pulmonary HTN related to lung disease increases RV afterload & can lead to R heart failure
Causes: COPD, PE, CF, interstitial lung dz, pneumoconiosis
R heart failure d/t pulm dz
Describe the clinical presentation of cor pulmonale
Dyspnea, orthopnea & PND rarely sxs of isolated RF, tussive or effort related syncope d/t inability of RV to deliver blood to L side, sxs of right HF
Ascites, peripheral edema
Describe the treatment for cor pulmonale
Treat underlying pulm dz
Oxygenation >90-92%
Diuretics effective in treating volume overload d/t right HF
Pulmonary vasodilators
Describe the 4 major types of A-fib
Paroxysmal: starts spontaneously & stops within 7 days
Persistent: duration 7+ days
Long-standing persistent: 1+ year
Permanent: persistent AF who have made decision with provider to stop attempts to control rhythm
Describe the sxs of a-fib
asymptomatic, fatigue, palpitations, lightheadedness, SOB, chest pain, anxiety, reduced exercise capacity, stroke
Describe the etiology of a-fib
Rapid firing ectopic foci mainly from pulmonary veins that overrides the SA nodes, AV node receives 500+ and allows only some to pass (120-180 bpm)
Impaired atrial contraction - decreased preload & CO - remodeling of atrium (less likely to spontaneously return to NSR)
Describe the two major categories of a-fib treatment (technically 3)
Rhythm control:
- cardioversion (required in persistent AF, preferred in symptomatic paroxysmal, urgent if unstable)
- antiarrhythmic drugs: propafenone, flecainide, amiodarone (Many AEs)
- catheter ablation (1st or after AAD)
Rate control:
- B-blocker: metoprolol
- Non-DHP Ca Channel blocker: diltiazem, verapamil
- can add digoxin if not effective
Anticoag:
- Vit K antagonist (Warfarin)
- Direct acting: Factor Xa (Xarelto, Eliquis), antithrombin inhibitor (Pradaxa)
Describe the EKG of a-fib
irregularly irregular appearance of QRS complex, absence of discrete P waves
Describe the EKG of a-flutter
atrial rate 250-350 bpm, often conducts to ventricles with 2:1 AV block creating a regularly tachy at 150 bpm, atrial “sawtooth”
Describe the CHADS(2) VASc score
Thromboembolic risk