Cardiac Diseases - HF, Tumors, IHD, CAD, Arrhythmias Flashcards
Relate the following factors in normal systolic function:
- stroke volume and preload
- stroke volume and afterload
- effect on SV of increasing preload and afterload
stroke volume is greater than preload and less than afterload; increasing preload will increase SV, increasing afterload will decrease SV
CHF
Symptoms AND signs resulting from cardiac dysfunction.
The dysfunction may be caused by damage to the heart (rheumatic HD, MI, endo/myocarditis, hypertrophy, etc.) or external forces that are preventing the adequate flow of blood from heart to the peripheral organs. If the apical impulse is displaced or enlarged = CHF diagnosis.
Why is dilation bad?
it increases afterload, which decreases stroke volume, which leads to hypoperfusion and cardiac dysfunction (CHF)
How is ejection fraction calculated?
(SV/EDV) * 100
Aldosterone
Tells kidneys to retain sodium; causes H2O retention.
RAAS activity goes up with heat-.
Plasma ALD concentration (PAC) should be about 50; in HF patients it’s in the hundreds because kidneys are hypoperfused and turn on RAAS.
What are the characteristics that would make you think CHF?
- low cardiac output
- abnormal retention of water and sodium by RAAS activity
- signs and symptoms of pulmonary and systemic congestion
What drug is the best treatment for CHF?
ACE-inhibitors
Diuretics don’t prolong survival they just make people feel better
Why is bed rest good for HF patients?
Patients with CHF have overactivity of the RAAS, so they already have too much renin and ALD in circulation. When you stand up, renin and aldosterone both increase, which causes water retention and increased BP/afterload/decreased SV, more cardiac dysfunction. Bed rest lets renin and ALD decrease, also BV. Bed rest (with elevated legs) also increases preload which stretches the atria and releases ANP, causing release of sodium and decrease in BV.
Pro-inflammatory nature of CHF
exact etiologic mechanism unknown but it has a lot to do with oxidative stress of hypoperfused organs, circulating cytokines (TNF and IL-6 are known elevated in pts with HF; also AT-II can turn on pro-inflammatory cytokines), and chronically elevated ALD is toxic to myocardium and causes fibrosis
What is the simple approximation of heart failure?
pump failure - which means there’s not enough blood where it needs to be, and it backs up meaning too much is where it is not needed
Normal ranges for: CVP LVEDP LVEDV SV EF LVESV
CVP: 2-8mmHg LVEDP: 4-12mmHg LVEDV: 65-240mL SV: 55-100mL EF: 50-75% LVESV: 15-145mL
What does it mean when the following are elevated? LVEDP LVEDV SV EF LVESV
LVEDP - HF because blood was leftover from previous cycle
LVEDV - HF because blood was leftover from previous cycle
SV - increased contractility
EF - increased contractility
LVESV - HF because SV wasn’t high enough
General Principles about HF:
- Initial sx of HF?
- What percent reduction in SV is threshold for HF?
- What’s wrong with acute uncompensated aortic regurgitation?
- Is mitral valve regurgitation a cause or sx of HF?
- When is the heart murmur for: mitral stenosis? mitral regurg?
- When is the heart murmur for: aortic stenosis? aortic regurg?
- initial sx is dyspnea on exertion
- 25% reduction in SV is threshold for HF sx
- problem with SAUAR is that it’s a surgical emergency
- mitral valve regurgitation can be EITHER a cause or sx of HF
- Mitral stenosis = diastolic murmur; mitral regurgitation = systolic murmur
- Aortic stenosis = systolic murmur; aortic regurgitation = diastolic murmur
Biggest symptoms of LHF and RHF:
LHF = dyspnea, progressing to orthopnea and PND, fatigue RHF = edema of feet, progressing to ankles and legs, abdominal distention
Biggest signs of LHF and RHF:
LHF = bibasilar pulmonary crackles, tachycardia, S3, LE edema RHF = LE edema, JVD, HP, ascites
What is the difference between edema due to RHF and edema due to LHF?
RHF = buildup of venous pressure LHF = fluid overload edema because RAAS more active when CO decreases (pump failure)
What causes pulmonary edema?
increase in pulmonary capillary pressure:
>20mmHg: transudative interstitial edema
>25mmHg: transudative alveolar edema, associated with wet crackles
Diastolic heart failure
noncompliant left ventricular walls that impair diastolic filling
Cor pulmonale (CP)
RHD due to some problem with blood being pumped to the lungs–could be parenchymal disease, pulmonary HTN, LHF, etc.; can progress to HF but many more patients have RHF due to LHF than due to cor pulmonale because most patients with CP are compensated
Why do patients with LHF (and not RHF due to CP) get orthopnea/PND?
orthopnea and PND arise from the increased venous return when lying back which exacerbates the LHF: more venous return means more blood that can’t be pumped out and backs up into the lung, causing edema and difficulty breathing. This doesn’t occur in CP because the RH CAN’T pump out more blood so the venous return backs up into the body (ascites, LE edema) instead of lungs and you don’t really see breathing problems
Major findings of:
LHF
RHF
mitral stenosis
LHF - wet crackles
RHF - JVD, HM, ascites, LE edema
mitral stenosis - diastolic murmur/rumble, dyspnea on exertion
Peripartum cardiomyopathy (PPCM)
type of new HF in previously healthy peripartum patient that’s not well understood but comes from fragment of prolactin, sFLT1, and other pregnancy-related hormonal and immune system imbalances that play a role
Types of shock: Distributive Obstructive Cardiogenic Hypovolemic Which is the most common?
Distributive = when BV is distributed too widely, like in inflammation; can be septic or non-septic but septic is the most common Obstructive = when the blood can't be pumped from the heart because something is in the way, like a PE or cardiac tamponade Cardiogenic = when the heart can't pump because of muscle failure, like in MI Hypovolemic = when there is not enough BV to perfuse, like in hemorrhage
Heart failure with preserved ejection fraction
Heart is failing because the ventricular wall is too hypertrophied/non-compliant to fill enough (so low SV), but it’s still able to pump well enough to maintain the same fraction of blood ejected in each contraction. This is diastolic dysfunction and the hypertrophy is a form of compensation. The failure comes when systolic function falls below the required threshold for SV, and can then quickly decompensate when EF falls (:systolic dysfunction)
