Cv 13: Acute Heart Failure

Front 1

What do venous return curves show?

Back 1

- Central venous pressure (y) vs Cardiac output (x): negative relationship
- Reflects circulatory volume, peripheral vascular resistance, and venous / arterial compliance

Front 2

What does a venous return curve tell us would happen if the CO was 0?

Back 2

- Volume of blood contained within circulation, as well as compliance of both vascular trees, will exert a pressure (max central venous pressure)
- Pressure decreases as CO increases

Front 3

What happens to the central venous pressure as cardiac output increases?

Back 3

Central venous pressure decreases

Front 4

How can we relate venous function and cardiac function?

Back 4

- CO (y) vs Central Venous pressure (x)
- Vascular function has neg slope
- Cardiac function has pos slope
- Where they intersect tells you CO and Central Venous Pressure

Front 5

What will happen to cardiac function and venous function if the central venous pressure increases through an increase in blood volume, peripheral resistance, or comliance?

Back 5

- Venous return curve shifts to right
- This increases cardiac function through increases in contractility
- Meet new equilibrium point of CO and Central Venous Pressure

Front 6

What is the Frank-Starling Relationship?

Back 6

Connects force and muscle fiber length

Front 7

What happens as a muscle fiber is stretched?

Back 7

Greater number of myosin-actin cross-bridges available
- Greater force

- At some point, fibers can be stretched too far to surpass the maximal length where optimal cross-bridging no longer occurs and force begins to decrease

Front 8

What components determine Cardiac Output?

Back 8

- Intrinsic factors: HR and Contractility
- Extrinsic factors: Preload and Afterload

Front 9

What happens to the cardiac function curve and equilibrium point if contractility is increased?

Back 9

- Cardiac function curve shifts up and to left to achieve higher CO with no change in central venous pressure
- Gradual reduction in central venous pressure occurs to meet new equilibrium point (↑CO and ↓Central Venous Pressure)

Front 10

How does an ↑HR affect CO for a healthy person vs a failing heart?

Back 10

- Healthy person: ↑HR will ↑CO with little change in SV
- Failing heart: ↑HR will decrease ability of heart to fill during diastole, leading to ↓SV

Front 11

Why is tachycardia a good clinical finding to help gauge severity of heart failure?

Back 11

Heart has no other way to generate cardiac output except by increasing its rate

Front 12

How does the venous return curve change with dilation / constriction?

Back 12

- Vasodilation: for same CO, afterload is decreased, flow through systemic circulation is enhanced, and more blood remains in venous circulation (increases venous pressure)
- Vasoconstriction: for same CO, more blood remains in arterial circulation and venous pressure decreases

Front 13

Why might you use an inotropic drug in acute heart failure?

Back 13

Stimulates contractility by increasing intracellular Ca2+ (in order to increase SV)

Front 14

What drugs can be used to increase contractility (pos. inotropes) in acute heart failure?

Back 14

- Dobutamine
- Epinephrine
- Norepinephrine

Front 15

What is the mechanism of Dobutamine, Epinephrine, NE in acute heart failure?

Back 15

- Bind β1 receptor (agonists)
- G-protein coupled receptor → stimulates AC
- ↑cAMP → activates PKA
- Phosphorylates L-type Ca2+ channel, Ryanodine Receptor, and Phospholamban → ↑intracellular Ca2+
- ↑Contraction

Front 16

How is the phosphorylation of L-type Ca2+ channel, Ryanodine Receptor, and Phospholamban controlled?

Back 16

- Pos inotropes like Dobutamine, Epinephrine, NE phosphorylate them to increase contraction
- Phosphodiesterases degrade cAMP to inhibit contraction
- Milrinone = PDE inhibitor, stimulates contracting too

Front 17

How can you measure the cardiac output?

Back 17

- Cardiac catheterization lab
- Use Swan-Ganz Catheter to collect true central venous O2 sample
- CO measurement is calculated by Fick principle

Front 18

What is the Fick Principle?

Back 18

- Principle in conservation of mass
- O2 conc. in pulmonary vein has to equal O2 conc. in pulmonary artery + O2 absorbed by capillaries from alveoli
- Blood flow will be proportional to O2 consumption
- Blood flow will be inversely proportional to difference in O2 content between pulmonary vein and artery

Front 19

What is the equation to calculate CO (Fick Principle)?

Back 19

CO = O2 consumption / ([Arterial O2] - [MVO2])

MVO2 = mixed venous O2 saturation

Front 20

What happens to the cardiac function curve in heart failure?

Back 20

Shifts down --> can't achieve same CO w/o increasing central venous pressure (and sometimes still can't achieve same CO d/t decreased contractility)

Front 21

In heart failure, there is a decrease in CO, a compensatory increase in central venous pressure, what can this cause?

Back 21

Filling pressures are too elevated and cause pulmonary edema

Front 22

What are causes of acute heart failure?

Back 22

- MI / CAD
- Valvular disease
- Viral or bacterial CM
- Myocarditis
- Thyroid disease
- Sepsis
- Arrhythmias (ventricular and SVT and bradyarrhythmias-heart block)
* Exacerbation of chronic heart failure

Front 23

What are the two questions you need to ask when seeing a patient you see with heart failure?

Back 23

- Do they have evidence of volume overload?
- Do they have adequate perfusion to meet their metabolism?

Front 24

How can you classify patients with heart failure? What is best / worst / most common?

Back 24

- Warm and Dry (this is the goal)
- Warm and Wet (most common)
- Cold and Dry (think hemorrhage)
- Cold and Wet (10%, highest mortality)

Front 25

Which heart failure classification has the highest mortality?

Back 25

Cold and Wet

Front 26

What is the ideal classification of a patient w/ heart failure?

Back 26

Warm and Dry

Front 27

What classification of a patient w/ heart failure would make you think of a hemorrhage?

Back 27

Cold and Dry

Front 28

What is the most common presentation of a patient w/ heart failure?

Back 28

Warm and Wet

Front 29

What symptoms do you see in a "warm and dry" patient?

Back 29

- Dyspnea
- Lower extremity edema
(Best)

Front 30

What symptoms do you see in a "warm and wet" patient?

Back 30

- Increased weight (retaining fluids)
- Elevated JVD
- Peripheral edema
- Dyspnea / orthopnea / rales
(Most common)

Front 31

What symptoms do you see in a "cold and dry" patient?

Back 31

- Dry mucous membranes
- Tachycardia
- Hypotension
- Cold extremities
(Consider hemorrhage)

Front 32

What symptoms do you see in a "cold and wet" patient?

Back 32

- Hypotension
- Tachycardia
- Cold extremities
- Elevated JVD
- Dyspnea / orthopnea
(Highest mortality)

Front 33

What are some techniques for assessing patients with Acute Heart Failure?

Back 33

- Echo
- Swan-Ganz Catheter
- Physical exam
- Lab testing (chest xray, BMP, Nt-pro BNP, troponin, ECG)

Front 34

What would you be looking for when doing an echo on a patient w/ possible acute heart failure?

Back 34

- ID cause of acute decompensation by looking at wall motion and valvular (dys)function
- Can estimate: RA pressure, CO, LA pressure (E/e'), LV dimensions and volumes
- Monitor progress of therapy
- Efficacy of LV ejection during systole (EF)
- Estimate CO w/ Doppler measurement of flow across LV outflow tract or mitral valve if we know HR

Front 35

How can heart failure be graded?

Back 35

Severity of EF:
- 45-50% = mild
- 35-44% = moderate
- <35% = severe

Front 36

What is the method of a Swan-Ganz Catheter?

Back 36

- Catheter has a balloon at tip, which assists in moving catheter through RA, RV, and PA
- Record hemodynamic tracings and pressures in each location
- Continue catheter until PA waveform looks blunted and Mean Pulmonary Capillary Wedge Pressure (PCWP) is recorded
- Help measure CO

Front 37

What does the Pulmonary Capillary Wedge Pressure (PCWP) represent?

Back 37

Measures the pressure exerted by pulmonary venous system
- Assist in assessing the volume status of a patient
- Indirect measurement of LV EDP

Front 38

When should Swan-Ganz Catheterization be used? Does it help outcomes?

Back 38

- Uncertain fluid status, perfusion, systemic or pulmonary vascular resistance
- Hypotension or worsening renal function
- Evaluation for VAD or transplant
- Presumed cardiogenic shock
- Severe clinical decompensation w/ uncertain hemodynamic profile
- Apparent inotrope dependence or refractory symptoms

- Does not improve outcomes (diagnostic)

Front 39

What physical exam techniques should be used on a patient suspected of acute heart failure?

Back 39

- Vitals: BP, HR, weight
- JVD
- Rales
- Orthopnea
- Extremities (cold vs warm)
- Peripheral edema

Front 40

What does an elevated JVD tell you about a patient?

Back 40

Elevated volume status ("wet")

Front 41

What does the presence of Rales tell you about a patient?

Back 41

- Not often present in patients w/ chronic heart failure d/t lymphatic compensation
- May be seen in warm and wet presentation

Front 42

What does orthopnea tell you about a patient?

Back 42

- Useful for determining volume status
- More commonly in "wet" presentation

Front 43

What does peripheral edema tell you about a patient?

Back 43

- Useful for determining volume status
- More commonly in "warm and wet" presentation

Front 44

Why would you do a chest x-ray on a patient you suspect of acute heart failure? What should you look for?

Back 44

Look for:
- Interstitial edema
- Pleural effusion
- Pulmonary vascular congestion
- Heart size

Front 45

Why would you do a basic metabolic panel on a patient you suspect of acute heart failure? What should you look for?

Back 45

- Renal function is often worse in presence of renal venous congestion and hypoperfusion secondary to impaired cardiac function
- Look for elevations in serum creatinine and hyponatremia

Front 46

Why would you do a Nt-pro BNP on a patient you suspect of acute heart failure? What should you look for?

Back 46

Peptide marker of elevated filling pressures

- Best outcome if it decreases >30%
- Next best outcome if it changes <30%
- Worst outcome if it increases >30%

NT-proBNP: N-terminal-pro-brain natriuretic peptide

Front 47

Why would you assess troponin levels in a patient you suspect of acute heart failure? What should you look for?

Back 47

- Marker of cardiac myocyte injury
- Increase in troponin is associated with a 3-fold increase in patient's in hospital mortality

Front 48

Why would you do an EKG on a patient you suspect of acute heart failure? What should you look for?

Back 48

- Assess for arrhythmias or acute coronary syndrome
- Could be cause for patient's presentation

Front 49

How can you reduce preload to treat a patient w/ acute heart failure?

Back 49

* Diuretics (especially loop - furosemide, bumetanide, toresmide)
- If severe, may use w/ thiazide diuretic too (IV chlorothiazide or oral metolazone)

Front 50

What is the mechanism of Loop Diuretics?

Back 50

Inhibits Na/K/2Cl transporter

Front 51

How should diuretics be administered to a patient w/ acute heart failure?

Back 51

- Loop (furosemide): IV as bolus or continuous infusion
- If severe volume overload, combine w/ thiazide diuretic (chlorothiazide IV or oral metolazone)

Front 52

How can you reduce afterload to treat a patient w/ acute heart failure?

Back 52

* Vasodilators (nitroprusside, nitroglycerin, neseritide)

Front 53

What is the benefit of decreasing afterload in patients w/ acute heart failure?

Back 53

- Pressure in aorta is decreased
- Valve will open earlier
- Allows more blood to be ejected w/ each stroke

Front 54

What inotropes can be used in acute heart failure?

Back 54

- Dobutamine
- Milrinone
- Dopamine
- Levosimendan (not in US)

Front 55

What are the effects of inotropes in patients w/ acute heart failure?

Back 55

** Only for Cold and Wet patients refractory to other therapies **
- ↑ Myocardial contractility via stimulation of β-adrenergic receptors or through signaling to increase intracellular Ca2+
- Improves short-term hemodynamics, but worsen short term survival
- ↑ O2 demand which promotes myocardial ischemia

Front 56

What are the risks of using inotropes in patients w/ acute heart failure?

Back 56

- May promote myocardial ischemia by increasing O2 demand (via increased contractility)
- Increased risk of tachyarrhythmias
- Hypotension

Front 57

Which kind of patients can use inotropes for acute heart failure?

Back 57

** Only for Cold and Wet patients refractory to other therapies **

Front 58

What are the mechanisms of the inotropes used for acute heart failure?

Back 58

- Dobutamine - β agonist
- Milrinone - PDE3 inhibitor
- Dopamine - Mixed α and β agonist depending on dose
- Levosimendan (not in US) - sensitizes myofilaments to Ca2+ and opens K+ channels in vasculature

Front 59

What mechanical support can be given to patients w/ acute heart failure?

Back 59

- LVAD
- Tandem heart

Front 60

Is the Ejection Fraction always indicative of state of heart failure?

Back 60

No - a patient can have a "normal" EF and be in acute decompensated heart failure

Front 61

What are the PA catheter findings for Cold and Wet in acute heart failure?
- SVR
- CVP
- PCWP
- LV EDP
- CO / CI

Back 61

- SVR: ↑
- CVP: ↑
- PCWP: >18 mmHg
- LV EDP: ↑
- CO / CI: <2.2 L/min

Front 62

What are the PA catheter findings for Warm and Wet in acute heart failure?
- SVR
- CVP
- PCWP
- LV EDP
- CO / CI

Back 62

- SVR: ↓ / normal
- CVP: ↑
- PCWP: ↑
- LV EDP: N/A
- CO / CI: normal

Front 63

What are the PA catheter findings for Cold and Dry in acute heart failure?
- SVR
- CVP
- PCWP
- LV EDP
- CO / CI

Back 63

- SVR: ↑
- CVP: ↓ / normal
- PCWP: ↑
- LV EDP: ↑
- CO / CI: ↓

Front 64

What are the PA catheter findings for Warm and Dry in acute heart failure?
- SVR
- CVP
- PCWP
- LV EDP
- CO / CI

Back 64

- SVR: ↓
- CVP: ↓
- PCWP: ↓
- LV EDP: ↓
- CO / CI: ↑ / normal

Front 65

What does a high/normal/low SVR tell you about the type of Acute Heart Failure? What is this a measure of?

Back 65

↑ SVR: Cold
↓ SVR: Warm

SVR ~ Afterload

Front 66

What does a high/normal/low CVP tell you about the type of Acute Heart Failure? What is this a measure of?

Back 66

↑ CVP: Wet
↓ CVP: Dry

CVP = Central Venous Pressure

Front 67

What does a high/normal/low PCWP tell you about the type of Acute Heart Failure? What is this a measure of?

Back 67

↓ PCWP: warm and dry (this is the goal)
↑ PCWP: all others
↑ >18 mmHg: cold and wet

PCWP = wedge pressure (~LA pressure; normal is about 10-12 mmHg)

Front 68

What does a high/normal/low LV EDP tell you about the type of Acute Heart Failure? What is this a measure of?

Back 68

- ↑ LV EDP: cold
- ↓ LV EDP: warm and dry (goal)

Front 69

What does a high/normal/low CO / CI tell you about the type of Acute Heart Failure? What is this a measure of?

Back 69

- ↑/normal: warm and dry (goal)
- normal: warm and wet (most common)
- ↓: cold and dry
- ↓ <2.2 L/min: cold and wet

Front 70

How does hemoconcentration affect a patient with acute heart failure? How is this achieved?

Back 70

- Worsening renal function (↓GFR)
- Better survival
- Higher doses of loop diuretics → lose more weight/fluid → greater reduction in filling pressures

Front 71

What kind of patient will have congestion at rest?

Back 71

Wet patient

Front 72

What kind of patient will have low perfusion at rest?

Back 72

Cold patient

Front 73

What are the signs/symptoms of congestion, or being "wet"?

Back 73

- Orthopnea / PND
- JVD
- Ascites
- Edema
- Rales (rare)

Front 74

What are the signs/symptoms of low perfusion at rest, or being "cold"?

Back 74

- Narrow pulse pressure
- Sleepy
- Low serum Na+
- Cool extremities
- Hypotension w/ ACE-I
- Renal dysfunction

Front 75

How do you definitively diagnose someone as "dry"?

Back 75

PCWP < 18 mmHg AND
RA pressure < 8 mmHg

Front 76

How do you definitively diagnose someone as "wet"?

Back 76

PCWP > 18 mmHg OR
RA pressure > 8 mmHg

Front 77

How do you definitively diagnose someone as "warm"?

Back 77

Cardiac Index > 2.2

Front 78

How do you definitively diagnose someone as "cold"?

Back 78

Cardiac Index < 2.2

Front 79

What is cardiac index a measure of?

Back 79

Hemodynamic parameter that relates CO to body surface area (thus relating heart function to size of individual)

Front 80

What are the hemodynamic goals?
- RA
- PCW
- SBP
- SVR
- CO

Back 80

- RA < 8 mmHg (= dry)
- PCWP = <16 mmHg (= dry)
- SBP > 80 mmHg
- SVR: not a goal, but if filling pressures are high, would reduce to 1000-1200
- CO: not a goal

Front 81

What are the requirements for inotrope use?

Back 81

- Advanced systolic heart failure + low output syndrome + hypotension
- Vasodilators either ineffective or contraindicated
- Fluid overloaded and unresponsive to diuretics or manifest deteriorating renal function

Front 82

How should you treat a patient that is "cold and wet"?

Back 82

- May need to "warm them up" (increase perfusion) before drying them out
- Diuresis will improve CO
- Diuresis may not be possible though if renal perfusion is severely impaired
- SBP >85 mmHg use Vasodilator
- SBP <85 mmHg use inotrope + IABP (intra-aortic balloon pump)

Front 83

How should you treat a patient that is "cold and dry"?

Back 83

- PA Catheter placement to evaluate filling pressures
- If PCWP <12 and RA <6 (=dry): discontinue diuretics, PO fluids
- If PCWP >16 they are really cold and wet
- If PCWP 12-16 + normal RA pressure: vasodilators, IABP (intra-aortic balloon pump), and inotrope are temporary fix; needs VAD / transplant eval

Front 84

Why can inotropes be harmful in acute decompensated heart failure?

Back 84

- Arrhythmias
- Hypotension
- Increased troponin release
- Increases in-hospital and 6 month mortality
- Does not shorten hospitalization

Front 85

What are the effects of increasing doses of vasodilators?

Back 85

- ↓ Afterload
- ↑ SV
- ↓LV EDP
- ↓ Preload
(all good things)

Front 86

How should you treat a patient that is "warm and wet"?

Back 86

- Improve symptoms by reducing filling pressures
** IV diuretics
- Adjunctive therapies do not improve outcomes

Front 87

What are the challenges of diuretic therapy?

Back 87

- Threshold drugs (adequate dose needed to get therapeutic effect)
- Long-trem loop diuretic administration leads to reduced natriuretic response
- Rebound - infrequent dosing may lead to Na+ retention
- Long term tolerance (tubular hypertrophy to compensate for salt loss)

Front 88

What should you do if diuretics are not relieving the "wetness" of a "wet and warm" patient?

Back 88

- Re-evaluate presence / absence of congestion
- Restrict Na+ and fluids
- Increase doses of loop diuretics (continuous infusion)
- Add second type of diuretic orally (metolazone or spironolactone) or IV (chlorothiazide)
- Ultrafiltration (like dialysis)

Front 89

What kind of patient would need Ultrafiltration? What are the perceived benefits?

Back 89

- Patient who is "wet and warm" but is not getting therapeutic effects from diuretics alone

Benefits:
- Removes both Na+ and free water (isotonic)
- May decrease neurohormonal activation
- Improves pulmonary and peripheral edema
- Allows for fluid removal rate to match plasma refill rate of 15 mL/min
- Allows for reduction in diuretic use

Front 90

What percentage of patients with Heart Failure survive 5 years? How does preserved / reduced ejection fraction affect their survival?

Back 90

- 60% of patients are dead after 5 years
- Preserved EF has slightly better survival, but not significantly so

Front 91

How do β-blockers affect systolic function?

Back 91

- Initially cause ↓ systolic function (days)
- By a few months they significantly ↑ systolic function (and work chronically)

Front 92

When should you avoid using β-blockers?

Back 92

Hypervolemic state (don't want to endanger CO)