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Flashcards in Heart Failure Cases Deck (69):
1

What is heart failure

A complex clinical syndrome  Result of any structural or functional cardiac disorder that impairs the ability of the ventricle to fill with or eject blood  NOT necessarily “congestive” heart failure  HF is a progressive disorder  There is tremendous clinical heterogeneity

2

Poor prognosis of outcomes for heart fail pts:

repeat hospitalizations

3

What intrinsic factors contribute to CO?

Contractility and heart rate

4

What extrinsic factors contribute to CO?

Preload and Afterload

5

Heart Rate effects of Cardiac Output Tachycardia______ diastolic filling time.

decreases --> issue bc in heart fail we increase HR bc we need more blood but this will decrease diastolic fill time thereby reducing CO

6

Why is it an issue for pts with diastolic dysfunction to have tachycardia?

bc the heart fills with blood during diastole, if we have tachycardia, we decrease time spent in diastole.

7

In heart fail pts, impaired contractility leads to inability to handle volume thus ______ increases

CVP

A image thumb
8

What is La Places law?

Wall stress = Pressure x radus/ 2x wall thickness

9

In heart fail, pt experiences increase pressure, as a result what happens to the heart?

(think about La Place's Law)

wall stress = Pxr/2h

h is wall thickness, as P increases, we would increase wall stress. To resist increase in wall stess, the heart with increas it's wall thickness, h, via hypertrophy. After a certian point, it cannot hypertrophy anymore and we end up with decreased CO

10

CO = HR x SV thus as heart beast faster, we should increase CO. But this isn't quite the case... why?

as HR increases, it has a shortened diastole, thus HR can affect SV (bc SV is determined by diastolic filling time)

11

If HR is increased enough to decrease SV, what happens to preload and afterload?

Preload will decrease in response to decreased SV... afterload can change to compensate for decreased SV

12

When does active reuptake of Ca+ back into teh SR occur?

Diastole

13

How can increase in HR be a bad thing for pt with heart fail?

Pt with tachycardia and heart fail is bad because these pts depend on a longer diastolic filling time to generate adequte SV. When we see heart fail pt with tachycardia, it means they have no other way to generate CO except increase in HR

14

The amount a contracting heart must overcome to eject blood into the vasculature

afterload

15

Assuming no change in CO, when vasculature is contracted, more blood remains in arterial circulation... What happens to venous pressure?

Venous pressure decreases with each stroke

16

When afterload is reduced via vasodialation, flow across the systemic circulation is enhanced and central venous pressure will....

Increase

17

As a failing heart dilates ts wall stress increases. _________ is a compensatory mech for chamber dilation

Ventricular hypertrophy

18

Diuretics work to decrease __________ in order to decrease afterload in heart fail pts with compensatory hypertrophy

LV end diastolic pressure

19

•Sodium content in diet
• Excessive fluid intake
• Renal failure

all contribute to increased:

Preload

20

• Uncontrolled Hypertension
• Pulmonary embolism
• Severely dilated ventricle

all contribute to

increased AFterload

21

•Increased metabolism
•Fever
• Infection
• Anemia
• Tachycardia
• Hyperthyroidism
• Pregnancy
•Slow heart rate

all contribute to

increased HR

22

Acute MI
• Negative
 Inotrope 
• Alcohol

all contribute to

decreased contractility

23

What are the key components of the cycle of congestion in AHF

Myocardial ischemia--> worsening HF--> elevated LVEDP--> increased wall stress adn increased functiona MR--> myocardial oxygen deman--> back to ischemia

24

Role of the physician in Acute Heart Fail pts. 

1. Identify the etiology of acute heart failure
2. Appropriately treat acute heart failure to achieve a stable hemodynamic equilibrium.
3. Reverse (if possible) the exacerbating stimulus.

25

Assesment we need to perform on pt with AHF

• History and Physical Examination
• Laboratory Testing
• Echocardiogram (Non-Invasive Imaging)
• Swan-Ganz Catheter (Invasive hemodynamics)

26

What are some key questions to ask for in pt history in pt with AHF?

What do you eat for breakfast, lunch, dinner, snack, restaurants?
Do you weigh yourself every day?
How far can you walk?
How many pillows do you sleep with? Do you wake up short of breath?

Any recent changes to your medication?
Do you have chest pain?

27

What types of murmurs will we hear on pt with AHF?

Mitral regurgitation (Don’t rule out papillary rupture)
Crescendo-decrescendo murmur of Aortic stenosis
S3 Gallop 
P2 “knock” suggests RV volume or pressure overload

28

P2 “knock” suggests 

RV volume or pressure overload

29

Crescendo-decrescendo murmur is classic for:

 Aortic stenosis

30

What are findings seen in AHF pts as far as:

jugular veins

pulmonary exam

pulse rates

Distended jugular veins
Pulmonary: Tachypnea, inspiratory crackles
Lower extremity edema
Decreased pulses intermittent pulses

31

Your attending tells you to get the BP of a pt recently admitted for AHF, you get a SBP of 110mmHg... is this concerning?

Hypotension: SBP <115 mmHg predictive of increased mortality on presentation
 

32

Pt with ACF will be 

hot and sweaty or cold and clammy

Bradycardic or tachypnic

Cold clammy skin
Tachycardia

33

What are the two best predictors of event free survival in AHF pts?

third heart sound and JVP... if we can't make these go away, prognosis is very bad. 

34

What is Brain natiuretic peptide or Nt-pro-BNP a marker of

 Produced in the atria and ventricles in response to stretch.

35

When we get a basic metabolic panel in AHF pts, what are we assessing? What are our key markers?

Assess renal function and electrolyte imbalance
Elevated BUN (>43mg/dL) and elevated Creatinine most predictive of increased risk of mortality.
 

36

Why do we perform a CBC in AHF?

 Evaluate for anemia or hemoconcentration
 

37

Chest X Ray is taken in pt with AHF to check for:

pulmonary edema

38

When we need to find out the mixed venous O2 saturation, where do we draw it from?

Drawn from PA catheter, <70%

39

Troponin levels are used for what purpose in AHF labs?

Risk Stratification and Diagnostic tool
Elevated troponin levels in HF are common and predictive of death

40

What is the significance of getting an Echo in pts with acute decompensation?

Assists in identifying the cause: Wall motion, valve dysfunction
Assist in patient risk stratification.
Can give some estimates of hemodynamics: 
Monitor progress of therapy.
Ejection Fraction can give a rough idea about cardiac function, however a 
patient can have a “normal “ EF and be in acute decompensated heart 
failur

41

What hemodynamic estimates do echo's provide?

Right Atrial Pressure
Cardiac Output
Left Atrial Pressure ( E/ e’)
Left ventricular dimensions and volumes

42

How beneficial is knowing EF in a heart fail pt?

Ejection Fraction can give a rough idea about cardiac function, however a patient can have a “normal “ EF and be in acute decompensated heart failure

43

When do we consider a PA catheter?

• Uncertain fluid status, perfusion, systemic or 
pulmonary vascular resistance
• Hypotension or worsening renal function with empiric therapy
• Evaluation of candidacy for VAD or transplant
• Presumed Cardiogenic Shock
• Severe clinical decompensation with uncertain 
hemodynamic profile
• Apparent inotrope dependence or refractory 
symptoms

44

Key signs and symptoms of congestion or 'wet' symptoms

Orthopnea/PND, JVD, Ascities, edema, rales

45

Evidence of low perfusion or 'cool' symptoms

narrow pulse pressure, sleepy, low serum Na+, cool extremeties, hypotensive w/ ACE inhibitor, renal dysnfunction

 

46

Wedge pressure translates to:

LV end diastolic volume

47

High Wedge pressure =
 

 

Too much volume in Left Ventricle

48

Too much volume in Left Ventricle =
 

a. Too much preload
b. Not enough stroke 
volume

49

Key findings in 'Dry' patient

PCWP < 18 AND RA PRESSURE < 8

50

key findings in 'wet' pt

PCWP > 18 OR RA PRESSURE > 8

51

Warm patient will have cardiac index:

WARM= CARDIAC INDEX> 2.2

 

52

Cold pt will have cardiac index:

COLD= CARDIAC INDEX < 2.2

53

Hemodynamic goal for Right Atrial Pressure: 

< 8 mm Hg 

54

Hemodynamic goal for Pulmonary Capillary Wedge 

< 16 mmHg 

55

Hemodynamic goal of Systolic Blood Pressure 

> 80 mmHg 

56

What is our hemodynamic goal for SVR?

SVR – not a goal in itself, but if diastolic filling 
pressures are high consider reducing to 1000-
1200 dynes/sec/cm. 

57

Cold and Dry is EXTREMELY RARE PRESENTATION
* REQUIRES PA CATHETER PLACEMENT TO 
EVALUATE FILLING PRESSURE
– PCWP<12 AND RA<6: 
– PCWP >16:
– PCWP 12-16 + RA PRESSURE NORMAL:
 


– PCWP<12 AND RA<6: DC DIURETICS, PO FLUIDS
– PCWP >16: PROFILE C
– PCWP 12-16 + RA PRESSURE NORMAL:
• VASODILATORS , IABP, AND INOTROPE ARE 
TEMPORARY FIX
• NEEDS VAD/ TRANSPLANT EVALUATION 

58

• 27 YO F, presents to PCP with 2 weeks of “no energy”, abdominal bloating, early satiety. 
• Had an completed an uneventful pregnancy 8 weeks prior
• Vitals: BP 86/62, HR 110 BPM, RR 18, afebrile, BMI 20
• PE: Tachycardic, regular, soft S1, prominent P2, II / IV HSM L MSB, PMI diffuse and laterally displaced
• No edema, pulses +1
• Labs reveal Na+ 129, ALT 134, AST 189, rest normal

Diagnosed with likely cholecystitis, RUQ US ordered.

On hospital day 2, develops respiratory distress, desaturates to 88% O2 sat 
on BiPap. 
• Subsequently requires intubation and mechanical ventilation

What do you want to do next? 

STAT Echo shows LVEF 18%, moderate – severe mitral regurgitation, LVEDd 
7.2cm. 
• PA Catheter placed:
 

59

You place a PA cath in a pt and get these results; which are concerning?

• PA Catheter placed:
• RA 25
• RV 55/28
• PA 54/32
• PAWP 30
• SVO2 28%

• PA Catheter placed:
• RA 25; normal is 0-5; this is elevated = wet
• RV 55/28; 28 correlates with RA ressure and this is fine
• PA 54/32: this is slightly elevateed
• PAWP 30; normal is 6-12; this is elevated meaning high filling pressure
• SVO2 28%; mixed CO; this is super low (normal is 70% or higher) so blood is circulating slow

60

Pt presents and your attending says he is in AHF; and it is Cold and Wet

What do you expect the PCWP to be?

What do you expect the CI to be?

 WET = CONGESTION (PCWP>18)

COLD = INADEQUATE PERFUSION (CI<2.2)

61

Tx for patient with ACF defined as Cold and Wet

 YOU MAY NEED TO WARM THEM UP BEFORE 
DRYING THEM OUT
Diuresis to improve CO, but may not be possible if renal perfussion is severely impaired
Use: vasodialtor (maybe inotrope) and check SVR and look at BP
 

62

For AHF pt we use the follow drugs, why?

Diuretics:

Vasodialtors:

Ionotropes:

 

Diuretics reduce fluid volume

VasoD will decrease preload or afterload

Ionotropes will augment contractility

63

Key drugs to tx 'wet' symptoms

Vasodialators: nitroprusside, nitroglycerin and nesiritide

64

Pt is 'Cold and Wet' with PCWP low or normal and decreased CI... what do you tx with?

Ionotropic drugs: dobutamine, milrinone, Ca sensitizers

65

Ionotropes are not always a great choice in AHF pts... what three things would suggest use of ionotropes?

1. Advanaced systolic HF + low output syndrome + hypotension

2. Vasodialtors are either ineffective or contraindicated
3. Fluid overload and non-responsive to diuretics or they get deteriorating renal dysnfuction

66

Why do we consider ionotropes 'double edeged swords' when tx heart fail pts?

Heart failure leads to impaired calcium handling 
Inotropes to increase calcium ... YET increased Calcium leads to increased work and arrhythmia

67

Phosphodiesterase inhibitor administered as an iv infusion
Considered an inodilator because it is an inotrope and a vasodilator
Increases contractility and decreases afterload
No significant increase in myocardial oxygen consumption

Milrinone

68

Side effects of Milrinone

Hypotension: Can be attenuated by with holding 
bolus, Arrhythmia, Tachycardia

69

Ultimately milrinone will:

Increases contractility and decreases afterload