1
Q
What is heart failure?
A
- disorder in which heart pumps blood inadequately, leading to reduced blood flow, and back up of blood in the veins and the lungs
- as the blood backs up b/c of diminishing CO, pressure in heart chambers and vessels distal to failing pumping chamber increase - creating edema
- add kidneys will respond by retaining fluid and salt
- the body becomes congested
2
Q
2 main forms of HF?
A
- systolic: heart contracts less forcefully and can’t pump out as much blood that is returned to it. As a result, more blood remains in the ventricles (still only 40% EF)
- diastolic: heart is stiff and doesn’t relax normally after contracting. Even though it may be able to pump a normal amt of blood out of the ventricles, the stiff heart doesn’t allow as much blood to enter its chambers from the veins. As in systolic dysfxn the blood returning to the heart then accumulates in the veins
- both forms of heart failure often occur together
3
Q
Why is there a cough in CHF?
A
- fluid collecting in lungs, in alveoli because of increase in pressure, fluid leaks out into pleural space and causes pleural effusion - increased pressure on lungs and fluid build up cause cough
4
Q
Common causes and risks of CHF in US?
A
- ischemic heart disease (62%)
- cigarette smoking (16%)
- HTN (10%)
- obesity (8%)
- diabetes (3%)
- valvular disease (older pts)
5
Q
What are key risk factors for heart disease?
A
- high blood pressure
- high LDL cholesterol
- smoking
- other risk factors:
diabetes, overweight and obesity, poor diet, physical inactivity, and excessive alcohol use (decrease contractility of the heart)
6
Q
What are more rare causes of HF?
A
- viral myocarditis: (infection of the heart muscle) - coxsackievirus B
- infiltrations of the muscle such as amyloidosis
- HIV cardiomyopathy
- CT diseases such as SLE
- abuse of drugs such as alcohol of cocaine
- pharm drugs such as chemo agents
- arrhythmias
- OSA (independent cause of HF)
7
Q
What determines pump function of the heart?
A
- electrical system
- heart muscle excursion - EF
- priming the heart: preload
- resistance to ejection: after load (PVR)
8
Q
What is cardiac arrest, what is it due to?
A
- cessation of normal circulation of blood due to failure of the heart to contract effectively. Medical personnel may refer to an unexpected cardiac arrest as a sudden cardiac arrest
- a cardiac arrest is different from (but may be caused by) a heart attack, where blood flow to the muscle of the heart is impaired
- arrested blood circulation prevents delivery of O2 to the body, lack of O2 to the brain causes LOC, which then results in abnorm or absent breathing. Brain injury is likely to happen if cardiac arrest goes untx for more than 5 minutes. Cardiac arrest is a medical emergency!!!
9
Q
Patho phys of CHF?
A
reduced force of contraction due to overloading the ventricle. In a healthy heart, increased filling of the ventricle results in increased force of contraction (by Frank-starlying law of the heart) and thus a rise in cardiac output In HF this mechanism fails, as the ventricle is loaded with blood to the pt where heart muscle contraction becomes less efficient. This is due to reduced abilty to cross-link actin and myosin filaments in over stretched muscle.
10
Q
What is a common cause of systolic dysfunction?
A
- CAD.
- it can impair large areas of the heart muscle because it can reduce blood flow to large areas of the heart
11
Q
Most common cause of diastolic dysfunction?
A
- inadequately tx high blood pressure. High BP stresses the heat because the heart must pump blood more forcefully than normal to force blood into the arteries against the higher pressure. Eventually, the heart’s walls thicken, then stiffen. The stiff heart doesn’t fill quickly or adequately so that with each contraction, the heart pumps less blood than it normally does
12
Q
What is worse, orthopnea or PND?
A
- orthopnea is presentation of severe CHF: can’t lay down because fluid fills up the lungs
- PND: earlier manifestation - wake up in middle of the night gasping for air
13
Q
Why are crackles heard inCHF?
A
- from the alveoli popping open, from surface tension inside, and from congestion in lungs from back up of pressure.
14
Q
How does the RAAS mechanism contribute to worsening CHF?
A
- decreased renal blood flow secondary to low CO triggers renin secretion by the kidneys
- aldosterone is released - this leads to increase of Na+ and then water retention
- preload increases
- worseing failure
15
Q
2 diff mechanisms that cause systolic LSHF? and examples of each
A
- impaired contractility:
1. MI
2. transient MI
3. chronic vol overload: mitral or aortic regurg
4. dilated cardiomyopathy - volume overload (increased preload)
1. mitrial insufficiency
2. aortic insufficiency
3. atrial/or ventricular septal defect
16
Q
2 diff mechanisms that cause diastolic LSHF? examples of each
A
- impaired ventricular relax:
1. LVH
2. hypertrophic cardiomyopathy
3. restrictive cardiomyopathy
4. transient MI - increased after load (pressure overload)
1. mitral stenosis
2. pericardial constriction or tamponade
3. aortic stenosis
4. uncontrolled HTN
17
Q
When does CHF occur?
A
when the pumping efficiency of the heart is so low that blood circulation cannot meet tissue needs
- reflects weakening of myocardium by various conditions which damage it in different ways:
1. coronary atherosclerosis
2. persistent high BP
3. dilated cardiomyopathy
4. valvular heart disease
18
Q
Mechanism of coronary atherosclerosis?
A
- clogging of coronary vessels with fatty buildup
- heart becomes increasingly hypoxic and begins to contract ineffectively
- myocardial ischemia occurs when myocardial availability to meet metabolic requirements just doesn’t happen (supply isn’t meeting demand)
- damage to endothelium occurs and this leads to decrease in nitric oxide and prostacyclin production (vasodilators), and increased enodthelin prod (vasoconstrictor) - this leads to vasoconstriction, vasospasm, and thrombosis
19
Q
What occurs in MI that leads to impaired myocardial contraction and cell death?
A
- intracellular acidosis - this leads to increased Na/H exchanged which leads to increased intracellular Na and then decreased Na/Ca exchange - to intracellular Ca overload - this is what causes impaired myocardial contraction and cell death
20
Q
Effects of MI?
A
- diastolic dysfxn: when a sufficient amt of myocardium is ischemic, then LVEDP rises (first indication of ischemia) so relaxation is impaired and myocardial compliance decreases
- systolic dysfxn: ischemia causes alterations that may range from minimal impairment to absence of movement (akinesis), may have compensation by surrounding areas of normal muscle
21
Q
Why does angina pectoris occur in heart disease? How might this lead to a MI?
A
- caused by a fleeting deficiency in blood delivery to the myocardium
- this may result from stress induced spasms of coronary arteries or from increased physical demands on the heart
- myocardial cells are weakened by temp lack of oxygen but don’t die
- This leads to an MI if there is a prolonged coronary blockage that leads to cell death, most areas of cell death are repaired with noncontractile scar tissue
22
Q
How can persistent high BP lead to CHF?
A
- aortic pressure is usually 80 mm Hg during diastole
- when aortic diastolic rises to 90 or more, the myocardium must exert more force to open the aortic valve and pump out the same amt of blood
- myocardium hypertrophies - and stress takes its toll and the myocardium becomes progressively weaker
23
Q
Difference b/t concentric and eccentric hypertrophy?
A
concentric: hypertophy of septum, overcomin the increased pressure and has better result of trying to compensate.
eccentric: dilated, not able to maintain relationship with chamber size (can’t keep original shape), not able to keep up, starting to fail (decompensating)
24
Q
What occurs in dilated cardiomyopathy?
A
- ventricles stretch and become flabby and myocardium deteriorates
- cause often unknown (autoimmune)
- drug toxicity: alcohol, cocaine, excess catecholamines, chemo agents
- hypothyroidism, and infalmmation of heart - CHF
- heart’s attempts to work harder result in increasing levels of Ca in cardiac cells which activates a Ca sensitive enzyme that initiates a cascade which switches on genes that cause heart enlargement.
- because ventricular contractility is impaired, CO is poor and the condition progressively worsens
- dilation is to accomodate stroke volume because excursion is poor
25
What is cardiomyopathy?
- progressive impairment of structure and function of muscular walls of the heart chambers
26
3 main types of cardiomyopathy?
- dilated
- hypertrophic
- restrictive
27
Dilated cardiomyopathy?
- ventricles enlarge and impair systolic function. Progressive LV enlargement leads to heart failure, ventricular arrhythmias and embolic complications
28
Hypertrophic cardiomyopathy?
- walls of ventricles thicken and become stiff and impair diastolic relaxation. The assoc rise in LV pressure is transmitted backwards leading to elev left atrial and consequently pulm capillary pressure
29
restrictive cardiomyopathy?
- uncommon, wall of ventricles become stiff, but not necessarily thickened due to infiltration of fibrotic myocardium. Has poor prognosis, will ultimately lead to CHF, leads to diminished output
30
Etiology of RHF?
- acute MI: inferior
- pulm disease: COPD, fibrosis, HTN
- cardiac disease: involving left or both ventricles
- LVF (most common cause of RHF)
31
Pathophys of RHF?
- decreased right side CO or increased pulm vascular resistance leads to increased right ventricular pressures
- as pressures rise, this leads to increased pressure in RA and venous system, and higher right atrium pressure - lead to JVP
32
Increased end systolic volume is usually caused by in RHF?
- reduced ventricular excursion
33
What causes decreased end diastolic volume in RHF?
- impaired ventricular filling (as occurs when the compliance of the ventricle fall - ex: when the walls stiffen)
34
Increase of ventricular volumes causes in RHF?
- reduction in stroke volume due to mechanical and contractile inefficiency
35
What will the PE show in RHF?
- may reveal pitting peripheral edema, ascites, and hepatomegaly.
- JVP is frequently assessed as a marker of fluid status, which can be eliciting hepatojugular reflux. If the right ventricular pressure is increased, a parasternal heave may present, signifying the compensatory increase in contraction strength.
36
In a pt with RHF, if you have them hold their breath what may you see?
- carotid pulse bounding
37
What is an abnormal JVP?
- greater than 3 cm (can do at any angle, easier to see with less of an angle)
38
Back up of fluids in RHF?
- backward failure of RV leads to congestion of systemic capillaries. This generates excess fluid accum in the body (peripheral edema or anasarca)
- affects the dependent parts of body first (foot and ankle swelling in people who are standing up, and sacral edema in people who predom are lying).
- nocturia: occurs with increased fluid reabsorption when lying
- ascites (fluid accum in abdominal cavity and hepatomegaly) may develop. Sig liver congestion may result in impaired liver fxn, and jaundice and even coagulopathy may occur
39
Common respiratory signs of LSHF?
- tachypnea, and increased work of breathing.
- rales or crackles heard initially in lung bases, and when severe, throughout lung fields suggest development of pulmonary edema (fluid in alveoli). Cyanosis which suggests severe hypoxemia, is a late sign of extremely severe pulmonary edema
40
How can LSHF be divided? Presentation?
- failure of left atrium, the left ventricle or both within the left circuit. The pt will have dyspnea on exertion and in severe cases, dyspnea at rest
- orthopnea, or PND
- easy fatigueability and exercise intolerance are common complaints related to resp compromise
- cardiac asthma or wheezing may occur
41
What is systolic dysfunction?
- failure of the pump fxn of the heart. It is characterized by a decreased ejection fraction (less than 45%). The strength of ventricular contraction is attenuated and inadequate for creating an adequate SV, resulting in inadequate CO
- in general, this is caused by dysfxn or destruction of cardiac myocytes or their molecular components
42
How can these myocytes be damaged?
- in congenital diseases such as duchenne muscular dystrophy, cells are affected
- also can be damaged by inflammation (myocarditis)
- toxins and pharm agents ( ehtanol, cocaine, doxorubicin, and amphetamines) cause intracellular damage and oxidative stress.
- most common mech is ischemia causing infarction and scar formation. Dead myocytes are replaced by scar tissue, deleteriously affecting the fxn of the myocardium. On the echo: manifest by abnorm wall motion or absent wall motion
43
Mechanism of systolic dysfunction?
ventricle is inadequately emptied, VEDP and volumes are increased. This is transmitted to the atrium and thence to pulm vasculature. The resultant increased hydrostatic pressure favors extravasation of fluid into the lung parenchyma, causing pulmonary edema
- 3rd heart sound (blood left over in ventricle)
- increased presure in pulm vasculature affects R side of the heart, and this gets transmitted to the systemic venous circulation and systemic capillary beds, favoring extravasation of fluids into the tissue of target organs and extremities, resulting in dependent peripheral edema.
44
What does diastolic dysfunction result from?
- from failure of ventricle to adequately relax and typically denotes a stiffer ventricular wall
- this causes inadequate filling of ventricle, and therefore results in an inadequate stroke volume
- the failure of ventricular relaxation also results in elevated end diastolic pressures and the end result is identical to the case of systolic dysfunction ( pulm edema in left heart failure, periph edema in R heart failure)
45
When will diastolic dysfunction manifest itself?
- may not manifest itself except in physiologic extremes if sysolic fxn is preserved. The pt may be completely asx at rest. However, they are exquisitely sensitive to increases in HR, and sudden bouts of tachycardia (can be caused by any little thing: fever, dehydration, tachyarrhythmias ( afib - may result in flash pulm edema). adequate control of rate is key to preventing decompensation ( b blocker)
- 4th heart sound
46
ACC/AHA working group - stages of HF?
- stage A: pts at high risk for developing HF in future but no functional or structural heart disorder (pre-heart failure - can prevent progression to overt sxs)
- stage B: a structural heart disorder but no sxs at any stage
- stage C: previous or current sxs of HF in context of an underlying structural heart problem, but managed with medical tx
- stage D: advanced disease requiring hospital based support, a heart transplant or palliative care
-
47
Goals for tx diastolic heart failure?
- tx precipitating factors and underlying disease
- prevent and tx HTN and ischemic heart disease
- surgically remove diseased pericardium
- improve LV relaxation
- ACE inhibitors
- CCBs
- regress LVH (ACEIs and ARBs) and aldosterone antagonists, BBs and CCBs
- maintain AV synchrony by managing tachycardia: BBs preferred, CCBs (2nd), digoxin (controversial)
48
How can we optimize circulating volume in diastolic heart failure?
- ACEI
- aldosterone antagonists
- salt and water restriction
- diuresis, dialysis, or plasmapheresis
- BB or ACEI
49
How can we prevent relapse by intensifying outpt follow-up?
- control BP
- dietary counseling (Na+)
- monitoring volume status (daily weights, and diuretic adj)
- institute exercise program
50
Chronic management goal of diastolic heart failure?
- prevent development of acute decompensated HF
- counteract the consequence of ventricular remodeling
- minimize pts sxs
- digoxin
- ACEI: captopril, lisinopril (all improve survival and quality of life in heart failure pts)
- BBs
- diuretics
- ARBs
- aldosterone antagonists, spironolactone K sparing diuretics
- meds not helping: AICD, cardiac transplantation, ventricular assist device
51
What should you look for on a PE if you suspect CHF?
- vital signs: BP, HR, RR, temp
- pallor: anemia
- cyanosis
- jaundice
- clubbing (kind of unusual)
- peripheral edema
- JVP
- cardiac impulse ( 3rd or 4th heart sounds)
52
What is the goal in acute decompensation?
- immediate goal is to re-establish adequate perfusion and O2 delivery to end organs
- Make sure ABCs are adequate
- immediate txs usually involve some combo of vasodilators sich as nitro, diuretics (furesemide) and possibly NIPPV
Cardiology
flashcards
Decks in class (20)
# Cards
-
Pathophys52
-
Pharm for ischemic heart disease52
-
Physiology of HTN47
-
Antihypertensives148
-
Cardiac cycle12
-
Congenital Heart Defects44
-
cardiac lab eval29
-
cardiac dx and invasive procedures40
-
cardiac stress testing23
-
ischemic heart disease82
-
CAD risk factors22
-
CHF52
-
Valvular disorders80
-
dysrhythmias74
-
infective endocarditis68
-
pericardial diseases28
-
antiarrhythmic drugs29
-
Meds and metabolic derangements (EKG effects)12
-
Cardiomyopathies39
-
Vascular diseases68
