Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

CV Quiz 2 > Heart Failure Cases > Flashcards

Heart Failure Cases Flashcards

(69 cards)

Start Studying
1
Q

What is heart failure

A

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

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

Poor prognosis of outcomes for heart fail pts:

A

repeat hospitalizations

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

What intrinsic factors contribute to CO?

A

Contractility and heart rate

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

What extrinsic factors contribute to CO?

A

Preload and Afterload

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

Heart Rate effects of Cardiac Output Tachycardia______ diastolic filling time.

A

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

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

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

A

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

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

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

A

CVP

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

What is La Places law?

A

Wall stress = Pressure x radus/ 2x wall thickness

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

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

(think about La Place’s Law)

A

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

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

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

A

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

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

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

A

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

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

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

A

Diastole

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

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

A

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

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

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

A

afterload

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

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

A

Venous pressure decreases with each stroke

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

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

A

Increase

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

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

A

Ventricular hypertrophy

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

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

A

LV end diastolic pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q
  • Sodium content in diet
  • Excessive fluid intake
  • Renal failure

all contribute to increased:

A

Preload

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q
  • Uncontrolled Hypertension
  • Pulmonary embolism
  • Severely dilated ventricle

all contribute to

A

increased AFterload

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q
  • Increased metabolism
  • Fever
  • Infection
  • Anemia
  • Tachycardia
  • Hyperthyroidism
  • Pregnancy
  • Slow heart rate

all contribute to

A

increased HR

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

Acute MI
• Negative
Inotrope
• Alcohol

all contribute to

A

decreased contractility

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

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

A

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

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

Role of the physician in Acute Heart Fail pts.

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

CV Quiz 2 (16 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions