Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

M2 Cardiology > 2. Heart Failure and Shock 2 > Flashcards

2. Heart Failure and Shock 2 Flashcards

1
Q

Define Shock

A

Clinical syndrome, underfilling of arterial system and low BP. usually lasts only a few hours. MAJOR problem is poor tissue perfusion.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Define heart failure

A

complex clinical syndrome that results from any structural or functional impairment of ventricular filling or ejection of blood. Impaired pump performance, also progressive deterioration of the heart.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

3 causes of shock

A
  1. hypovolemic
  2. distributive
  3. cardiogenic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Define hypovolemic shock

A

too little blood in the system. due to blood loss or fluid loss (endothelial damage ie burns, excessive secretion ie cholera, dehydration)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

define distributive shock

A

vasodilation. enough fluid in system, but the blood is in the wrong place. veins rather than arteries.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what could cause distributive shock?

A

sepsis (vasodilator actions of endotoxins, ie toxic shock)

vaso-vagal syncope

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

define cardiogenic shock

A

inadequate filling of the arteries caused by failure of the cardiac pump. could be due to MI (LV damage), valve rupture, PE, myocarditis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

consequences of shock?

A

multi-organ failure, if not treated soon pt will die

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what is the underlying disease that causes heart failure in most patients?

A

left heart failure, affects left ventricular function.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

reasons for left heart failure?

A

ischemic heart disease, HTN, both dilated and hypertrophic cardiomyopathies, aortic and mitral valve diseases.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

reasons for right heart failure?

A

chronic pulmonary disease (COPD, emphysema), pulmonary HTN, congenital heart disease.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what is backward failure

A

blood accumulates behind the heart, causing veins to be overfilled.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what is forward failure

A

too little blood flows out of the heart to provide for the needs of the body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what is ESPVR

A

end systolic pressure volume relationship. defines ventricular stiffness at the END of systole and is a measure of contractility/inotropy. pressure at the end of systole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what is EDPVR

A

end diastolic pressure volume relationship. defines ventricular stiffness at the END of DIASTOLE and is the measure of ability of ventricle to RELAX (lusitropy).
pressure at end of diastole.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Think through a cardiac pressure-volume loop.

A

start at end-diastole (bottom right). isometric contraction with no change in volume until hit point of AFTERLOAD. then decr volume with incr pressure with pumping of systole. hit ESVPR line at end systole, and have isovolumetric relaxation (line straight down). Then have change in volume with not much change in pressure until hit end-diastolic point and PRELOAD.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Starling’s law of the heart says what?

A

when the heart has more volume, it is able to do more work.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

which line moves with inotropic abnormalities?

A

the ESPVR line, slants more towards the volume axis. will cause forward failure because there is decreased Stroke Volume, and the pump is developing less arterial pressure in the periphery.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what would cause backward failure?

A

if the end diastolic point moves along the EDPVR line. will cause less blood to be moved out of veins because of incr filling pressure.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what problems will be caused by impaired relaxation?

A

forward failure: because of decr stroke volume and decr arterial pressure generated by the pump.
backward failure because of incr stiffness of the heart, incr filling pressure leads to backup in venous system.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

recap: backward failure. what is the main problem, and what happens in the R and L heart?

A

main problem: incr venous pressure.
L heart: blood backs up in pulm veins
R heart: blood backs up into peripheral veins.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

recap forward failure: what is main problem, and what is going on in R and L heart?

A

main problem: reduced cardiac output.
L heart: too little blood flows into systemic circ.
R heart: too little blood flows into pulm circ.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what would be symptoms of backward failure of the L heart?

A

incr pulmonary venous pressure, pulm edema (–> rales), dyspnea, orthopnea, paroxysmal nocturnal dyspnea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what would be symptoms of backward failure of the R heart?

A

incr systemic venous pressure, peripheral edema, ascites, pleural effusion, JVD.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what would be symptoms of forward failure?

A

decr tissue perfusion, eventually tissue damage (ie kidney necrosis, renal insufficiency)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

define dyspnea

A

difficulty breathing, largely due to incr work of breathing caused by stiff fluid-filled lungs. also may be due to arterial hypoxia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

define orthopnea

A

dyspnea that incr when patient reclines. gravity shifts blood from legs to lungs, incr fluid in lungs, incr dyspnea.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

define paroxysmal nocturnal dyspnea

A

awaken severely short of breath several hours after going to bed. fluid is resorbed from legs (edamatous) when they are elevated, re-enters systemic circ, incr blood volume.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

2 most common causes of systolic heart failure?

A

ischemic heart disease, dilated cardiomyopathy (familial, toxins, infections?)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

2 most common causes of diastolic heart failure?

A

hypertensive heart disease, hypertrophic cardiomyopathy.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

ultimately how can you tell the difference between systolic and diastolic heart failure?

A

ECHO.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

in systolic failure, what is the main problem?

A

heart does not EMPTY normally. HFrEF (heart failure with REduced ejection fraction)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

with diastolic heart failure, what is the major problem?

A

heart does not FILL normally. HFpEF or HFnEF (heart failure with Preserved ejection fraction or Normal ejection fraction)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

can you can you distinguish systolic from diastolic heart failure using hemodynamic measures/

A

NO, because a heart that cannot eject normally also cannot accept a normal venous return, so impaired ejection (systolic) also reduces filling. and a heart that cannot fill normally also cannot eject a normal stroke volume, so impaired filling (diastolic) also reduces ejection.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

so if the difference between systolic and diastolic failure is not hemodynamic, what is the difference?

A

ventricular architecture: eccentric hypertrophy v concentric hypertrophy.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

systolic failure: what does heart look like?

A

eccentric hypertrophy / dilatation. heart has grown and cannot get rid of blood.

37
Q

diastolic failure: what does the heart look like?

A

concentric hypertrophy. has grown in towards the center. cannot fill properly.

38
Q

how do we take a measurement to distinguish between systolic and diastolic heart failure?

A

take an ejection fraction.

39
Q

formula for ejection fraction?

A

EF = SV/EDV.

fraction of EDV that is ejected.

40
Q

systolic failure: what will ejection fraction be?

A

low.

41
Q

diastolic failure: what will EF be?

A

high or normal.

42
Q

since stroke volume is down in all patients with heart failure (both systolic and diastolic) what is actually the determinant of different ejection fractions in different types of failure?

A

the EDV: if big, then SV will be relatively small and EF is small -> systolic failure and eccentric hypertrophy (dilatation).
If EDV is small, then SV is relatively big and EF is bigger -> diastolic failure and concentric hypertrophy.

43
Q

in response to underfilling of the arterial system, what does the baroreceptor do?

A

activates sympathetic (adrenergic) NS and inhibits parasympathetic (cholinergic) NS.

44
Q

what will be the neurological response to exercise? (short duration, need to inc blood to muscles)

A

cardiac stimulation (inc HR, contractility), selective vasoconstriction (in organs not involved)

45
Q

what will be the neurological response to shock? (medium duration, experiencing decr volume of blood in arteries)

A

cardiac stimulation (HR, contractility), vasoconstriction (shunting in organs not involved), salt and water retention

46
Q

what will be the neurological response to heart failure? (long duration, experience impaired pumping, decr CO)

A

cardiac stimulation (HR, contractility), vasoconstriction (worsens towards failure), salt and water retention (worsens towards failure).

47
Q

what are the 2 elements of the neurohumoral response?

A

functional: short term, fight or flight
proliferative: longer term, growth.

48
Q

describe the functional component of the neurohumoral response

A

idea is to modify the function of existing structures.

  • cardiac stimulation via NE, AtII, vasopressin, endothelin, aldosterone.
  • vasoconstriction via NE, AtII, vasopressin, endothelin
  • water retention via vasopressin
  • sodium retention via selective vasoconstriction in kidneys
49
Q

describe the proliferative component of the neurohumoral response

A

modify cell size, shape, composition, cell survival. ex: more sarcomeres via transcriptional activation.

50
Q

what are the adaptive and maladaptive responses that are part of functional signaling as result of cardiac challenge (exercise, shock, heart failure). First part: cardiac stimulation

A
  • adaptive: incr contractility, incr relaxation, incr HR. yields incr CO.
  • maladaptive: more cytosolic calcium can lead to arrhythmias. incr cardiac energy demand can lead to cardiac myocyte death.
51
Q

what are the adaptive and maladaptive responses that are part of functional signaling as result of cardiac challenge (exercise, shock, heart failure). Second part: vasoconstriction

A
  • adaptive: incr afterload and maintain BP, inc tissue perfusion.
  • maladaptive: decr SV and CO, worsens forward failure failure, incr cardiac energy demand and promote cardiac myocyte death.
52
Q

what are the adaptive and maladaptive responses that are part of functional signaling as result of cardiac challenge (exercise, shock, heart failure). Third part: salt/water retention

A
  • adaptive: incr preload, maintain SV/CO. improves forward failure!
  • maladaptive: edema, anasarca, pulm congestion (ie worsens backward failure)
53
Q

what are the adaptive and maladaptive responses that are part of Proliferative signaling as result of cardiac challenge (exercise, shock, heart failure). ie, transcriptional activation

A
  • adaptive: more sarcomeres, normalize wall stress, maintain CO
  • maladaptive over time: cell elongation and remodeling. cell damage/apoptosis. decr energy supply and incr cardiac energy demand–> myocyte death.
54
Q

what is the major problem in dropsy?

A

fluid retention (not incr venous pressure)

55
Q

what are some consequences of energy starvation associated with heart failure?

A

Due to energy starvation:
-contractile protein interactions have depressed contractility, impaired relaxation.
-the Sarcoplasmic Reticulum Ca Pump (SERCA) doesn’t work as well, impairs relaxation, increases pump failure
-SERCA release channels cause depressed contractility. worsens pump failure.
-Plasma membrane ion channels less functional, cause arrhythmias, sudden cardiac death.
in SEVERE energy starvation, get cardiac myocyte death.

56
Q

what is the anticipated lifespan once heart failure becomes symptomatic?

A

if asx, can live indefinitely. once symptoms appear, can be a very quick decline. prob 10 years.

57
Q

cardiac myocytes: can they enlarge/hypertropy or incr in number/hyperplasia?

A

they can do hypertrophy but NOT hyperplasia. problem in heart failure where cardiac myocyte survival is reduced.
limited ability to replace lost myocytes is the major reason why heart failure is progressive.

58
Q

describe aortic insufficiency

A

dilated heart chamber. problem = increased stress during diastole when heart is relaxing. caused by blood leaking (backflowing) through the aortic valve.

59
Q

describe aortic stenosis

A

the ventricular cavity is smaller, thicker wall (hypertrophied). problem is increased stress during systole. caused by trying to squeeze blood through a narrowed aortic valve.

60
Q

Eccentric hypertrophy can be caused by at least 3 processes, what are they?

A

pathologies: (all cause dilatation)
- aortic insufficiency (valve issues)
- dilated cardiomyopathy (familial).
- ischemic cardiomyopathy (secondary pathology to ischemia)

61
Q

Concentric hypertrophy can be caused by at least 3processes, what are they?

A

pathologies:

  • aortic stenosis (valve issues)
  • hypertrophic cardiomyopathy (familial)
  • hypertensive heart disease (vascular HTN)
62
Q

the most common causes of heart failure in deve countries are what kind of disease?

A

BLOOD vessel diseases.

  • ischemic heart disease, occlusion of coronary arteries -> dilatation.
  • hypertensive heart disease, constrictin of systemic arterioles -> concentric hypertrophy
63
Q

what are the treatment strategies for ischemic heart disease?

A

smoking cessation, lower LDL cholesterol, treat HTN, prevent/treat diabetes.

64
Q

what are treatment strategies for hypertensive heart disease?

A

treat HTN, optimize body weight, exercise.

65
Q

what is the difference between pathological hypertrophy and physiological hypertrophy?

A

pathological is almost always progressive to heart deterioration and cardiac death, physiological hypertrophy does not have tendency to deteriorate/cause myocyte death. The difference is actually in the signalling pathways taken to achieve the hypertrophy - associated cytokines, extracellular messengers, MAP kinases, mechanical stress and cellular architecture.

66
Q

what happens at a molecular level with concentric hypertrophy?

A

volume of the LV barely changes, but the diameter thickens. length of individual myocytes doesn’t change. sarcomeres added in parallel.

67
Q

what happens at a molecular level with eccentric hypertrophy?

A

myocyte diameter stays constant but length increases. sarcomeres added in series.

68
Q

in the situation of aortic constriction (pathological hypertrophy), what are the molecular changes that happen at the myocyte level?

A

altered gene expression. have high amounts of the LOW ATPase-version of myosin heavy chain (B-isoform). leads to decr myocardial contractility.
also, less sarcoplasmic reticulum yields less intracellular calcium stores, less myocardial contractility.
Fetal phenotype.

69
Q

in the situation of aortic constriction (physiological hypertrophy), what are the molecular changes that happen at the myocyte level?

A

have high levels of the HIGH ATPase-version of myosin heavy chain (alpha-isoform). increases myocardial contractility. also have more SR, increases intracellular Ca stores and increases myocardial contractility.
Adult phenotype.

70
Q

in pathological hypertrophy, what is the main problem during systole?

A

progressive dilation/remodeling. dilatation incr wall stress, incr energy expenditure, reduces efficiency.

71
Q

when LV dilatation occurs in a pt with diastolic heart failure, it is usually caused by what?

A

MCI. diastolic heart failure is rarely complicated by progressive dilatation.

72
Q

what does an inotropic agonist do?

A

incr contractility.

73
Q

what are the benefits and harms of incr contractility?

A

benefits: incr BP, incr SV
harms: increased work worsens energy starvation.

74
Q

when giving inotropic meds, which is better, the harm (more energy starvation) or the benefit (inc BP, SV)?

A

they shorten survival, therefore off the market. they may incr mortality by inducing remodeling and maladaptive hypertrophy. (regardless of mech, they incr mortality)

75
Q

how do diuretics impact the heart function?

A

decr preload (beneficial), decr SV and CO (harmful).

76
Q

why must diuretics be given really carefully?

A

reducing preload also decr CO and BP; excessive diuresis can cause dangerous decr in CO and BP.

77
Q

in terms of the function of the heart, what do vasodilators do?

A

decr afterload.

78
Q

what are the harms and benefits to vasodilators?

A

benefit: decr afterload, inc SV. harm: decr SBP and tissue perfusion.

79
Q

what category of vasodilators doubled survival?

A

ACE inhibitors.

80
Q

what is unique about ACE inhibitors among other vasodilators?

A

they improve survival not by vasodilation but by inhibition of proliferative signaling (ie, inhibition of remodeling)

81
Q

what are the 3 classes of drugs that inhibit the proliferative signals that cause failing hearts to deteriorate?

A
  1. ACE inh
  2. angiotensin receptor blockers
  3. nitrates
82
Q

what happens if beta-blockers are given quickly?

A

they will worsen heart failure. they reduce contractility. but if they are given slowly, they are the best treatment we have.

83
Q

what is the main impact of beta-blockers?

A

they slow contractility, and inhibit remodeling.

84
Q

another class of drugs that inhibits remodeling in patients?

A

aldosterone antagonists.

85
Q

a non-drug way to treat heart failure?

A
  • cardiac resynchronization.
  • pace the heart in pts with AV block, sinus arrest, or severe sinus bradycardia.
  • provide overdrive suppression in patients with ventricular tachy
  • defibrillate in pts at risk for vfib.
86
Q

7 treatments that we have to improve survival in systolic heart failure?

A

inhibit proliferation:

  1. ACE inhibitors, ARBs
  2. nitrates
  3. beta-blockers
  4. aldosterone blockers

modify mechanical stress:

  1. resynchronization therapy
  2. artificial heart
  3. exercise
87
Q

what do we do to treat diastolic failure?

A

at this point, we have no idea. drugs that improve survival in systolic failure have less/no benefit in diastolic heart failure.

88
Q

why might therapy that improves prognosis in systolic heart failure fail to improve conditions with diastolic heart failure?

A

diastolic failure is rarely accompanied by remodeling, which is what a lot of therapies for systolic HF are aimed at preventing.

M2 Cardiology (32 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions