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Therapeutics > Exam 2 lecture 1 > Flashcards

Exam 2 lecture 1 Flashcards

1
Q

What are the two types of HF

A

Chronic HF
Acute HF

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2
Q

What are the types of chronic HF

A

Asymptomatic reduced ejection fraction
HFrEF
HFpEF

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3
Q

age related increase in likelihood of HF

A

60-69 -increases 5%
70-79- increases 7%
80-90- increases 10 %

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3
Q

5 year survival rate of HF

A

50%

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3
Q

What is the most common hospital discharge for patients >65

A

HF

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4
Q

definition of HF

A

An abnormality of myocardial function that is responsible for the failure of the heart to pump blood at a rate commensurate with the requirements of the metabolized tissues. (not a single disease, but a culmination of CV diseases such as HTN, CAD and myopathies)

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5
Q

Which diseases lead to left ventricular dysfunction

A

CAD, HTN, cardiomyopathy

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6
Q

What are non-cardiac factors that lead to HF

A

Endothelial dysfunction, neurohormonal activation, vasoconstriction and Na retention lead to remodelling of the left ventricle, leading to reduction in ejection fraction.

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7
Q

cure for HF

A

transplant

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8
Q

Two main types of HF

A

HFrEF
HFpEF

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9
Q

what is HFrEF

A

Impairment in diastolic dysfunction. leads to reduced contractility.

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10
Q

What is HFpEF

A

Impairment in diastolic dysfunction, leads to impairement in ventricular relaxation and filling. .

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11
Q

Difference between HFrEF and HFpEF

A

HFrEF- systolic dysfunction and LVEF<40%
HFpEF- diastolic dysfunction and LVEF>40%

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12
Q

causes of HFrEF

A

Dilated ventricle
- ischemia dilated CM (70% of cases)
- non-ischemia dilated CM
- cHTN, Thyroid, obesity, stress, cardiotoxins, myocarditis

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13
Q

cause of HFpEF

A

HTN (most common cause)

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14
Q

What are the 3 determinants of left ventricular performance

A

Preload
myocardial contractility
afterload

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15
Q

Preload meaning

A

Venous return; LV end- diastolic volume

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16
Q

myocardial contractility meaning

A

Force generated at any given LVED

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17
Q

Afterload meaning

A

Aortic impedance and wall stress

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18
Q

relationship between preload and stroke volume

A

Increase preload =increase SV

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19
Q

Frank starling curve X and Y axis names

A

Y- stroke volume
X- LV end diastolic pressure

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20
Q

pressure volume relationship X and Y axis names

A

Y- SV
X- afterload or SVR

21
Q

What drugs could reduce preload

A

diuretics (SGLT2)

22
Q

HF starts with a reduction in

A

Cardiac output.

23
reduced cardiac output in HF has what effect on the body
leads to a reduction in BP and organ perfusion.
24
What effect does HF reducing BP and organ perfusion have
body activate SNS, RAAS and elevates vasopressin to compensate. Also leads to increases in BNP and ANP (brain natriuretic peptide and arterial natriuretic peptide) which are good things
25
What do SNS, RAAS and vasopressin lead to
arrythmias, cell death and CM hypertrophy
26
Why would arrythmias happen with SNS
`catecholamines are released when SNS is activated. This pre disposes pts to arrythmias
27
How do SNS, RAAS and vasopressin increase affect afterload, preload and vasoconstriction? how do they affect renal perfusion, natriuresis and diuresis
Increase them decrease them
28
How does RAAS, SNS and vasopressin increase affect BP and HR
increases them
29
what are the compensatory responses to HF
1. increase in preload due to Na/H20 retention 2. Vasoconstriction 3. Tachycardia and increase in contractility (SNSactivation) 4. ventricular hypertrophy and remodelling
30
pros and cons if increase in preload due to Na/H2o retention
beneficial- optimize SV via frank-starling mechanism detrimental- pulmonary/systemic congestion and edema -increased MVO2
31
pros and cons of vasoconstriction as a compensatory mechanism
beneficial- maintain BP in face of reduced CO - shunt blood from non-essential tissue to heart detrimental- increase MVO2 increase afterload reduce SV and activates compensatory responses
32
pros and cons of tachycardia and increases contractility (SNS activation)
beneficial- maintains CO detrimental- increased MVO2 - shortened diastolic filling time -B receptor downregulation - ventricular arrythmia and cell death
33
pros and cons of ventricular hypertrophy and remodelling
beneficial- maintains CO reduces myocardial wall stress reduces MVO2 detrimental- diastolic and systolic dysfunction - risk of myocardial cell death and ischemia - risk of arrythmias and fibrosis
34
factors percipitating or worsening HF
lack of compliance with drug or diet uncontrolled HTN cardiac arrythmia A- fib Atrial flutter
35
are B blockers positive or negative ionotropes? verapamil? Diltiazem?
negative (reduce contractility) verapamil and diltiazem are also negative ionotropes
36
Name negative ionotropic drugs
Antiarrythmics (disopyramide, felcanide) B blockers non DHP CCB itraconazole
37
direct cardiac toxin drugs
Ethanol, cocaine, amphetamines and drugs that end in -nib and -mab
38
Name drugs that lead to water retention 1or Na retention
NSAIDs, COX-2 inhibitors, androgens, Estrogens, glucocorticoids, rosiglitazone, pioglitazone
39
clinical presentation of HF
SOB swelling of legs and feet cough with frothy sputum increased urination at night chronic lack of energy difficulty sleeping at night due to breathing problem confusion and/or impaired memory
40
major signs and symptoms of pulmonary congestion
exertional dyspnea (DOE) Orthopnea paroxysmal nocturnal dyspnea (PND) bendopnea
41
major signs and symptoms of venous congestion
Rales peripheral edema hepatojugular reflex JVD displacement of PMI
42
Why would an MI cause HF
infarct- death of tissue. scar tissue forms and scar does not contract as well.
43
Why would HTN cause HF
increases pressure and heart has to remodel itself
44
activation of SNS results in
peripheral vasoconstriction increased cardiac contractility and HR
45
BNP and NT-pro BNP nortmal levels
BNP<35 NT-pro BP<125
46
assessment to diagnose HF
1. clinical history physical exam ECG, labs 2. NT pro BNP>125 BNP>35 3. transthoracic echocardiogram
47
how to classify HF based of LVEF
LVEF<40%- HFrEF LVEF 41-49- HFmrEF LVEF>50- HFpEF
48
NYHA classicifaction of HF
class I- patients with cardiac disease but without resulting limitations of physical activity (asymptomatic) Class II- patients with cardiac disease resulting in slight limitations of physical activity Class III- patients with cardiac disease and limitations of physical activity Class IV- patients with cardiac disease and an inability to carry out any physical activity without discomfort
49
AHA classification of HF
class A- high risk of developing HF, no identified structural or functional abnormalities. No S/S of HF (HTN, CAD, DM) Class B- structural heart disease that is strongly associated with HF but no s/s of HF (NTHA class I) Class C- Current or prior sx of HF. Associated with underlying structural heart disease (NYHA II, III) Class D- Advanced structural heart disease and marked sx of HF at rest despite maximal medical therapy (severe symptoms) (NYHA IV)
50
Simple way to diagnose AHA classes
Class A- high risk (HTN, CAD, DM) no sx class B- asymptomatic LVD (NYHA I) class C- symptomatic HF (SOB, fatigue) NYHA II, III) Class D- Refractory end stage HF. (marked sx at rest despite maximal medical therapy)
51
Dietary measures for HF
Sodium should be restricted to 2-3 g/day patients with severe HF may be required <2g/day Etoh induced HF patiets- abstain totally in others 2 drinks/day in men and 1 drink / day in women fluid intake- restriction to <2L/day

Therapeutics (38 decks)

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