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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
Q

reduced cardiac output in HF has what effect on the body

A

leads to a reduction in BP and organ perfusion.

24
Q

What effect does HF reducing BP and organ perfusion have

A

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
Q

What do SNS, RAAS and vasopressin lead to

A

arrythmias, cell death and CM hypertrophy

26
Q

Why would arrythmias happen with SNS

A

`catecholamines are released when SNS is activated. This pre disposes pts to arrythmias

27
Q

How do SNS, RAAS and vasopressin increase affect afterload, preload and vasoconstriction?

how do they affect renal perfusion, natriuresis and diuresis

A

Increase them

decrease them

28
Q

How does RAAS, SNS and vasopressin increase affect BP and HR

A

increases them

29
Q

what are the compensatory responses to HF

A
  1. increase in preload due to Na/H20 retention
  2. Vasoconstriction
  3. Tachycardia and increase in contractility (SNSactivation)
  4. ventricular hypertrophy and remodelling
30
Q

pros and cons if increase in preload due to Na/H2o retention

A

beneficial- optimize SV via frank-starling mechanism

detrimental- pulmonary/systemic congestion and edema
-increased MVO2

31
Q

pros and cons of vasoconstriction as a compensatory mechanism

A

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
Q

pros and cons of tachycardia and increases contractility (SNS activation)

A

beneficial- maintains CO

detrimental- increased MVO2
- shortened diastolic filling time
-B receptor downregulation
- ventricular arrythmia and cell death

33
Q

pros and cons of ventricular hypertrophy and remodelling

A

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
Q

factors percipitating or worsening HF

A

lack of compliance with drug or diet
uncontrolled HTN
cardiac arrythmia
A- fib
Atrial flutter

35
Q

are B blockers positive or negative ionotropes?
verapamil? Diltiazem?

A

negative (reduce contractility)

verapamil and diltiazem are also negative ionotropes

36
Q

Name negative ionotropic drugs

A

Antiarrythmics (disopyramide, felcanide)
B blockers
non DHP CCB
itraconazole

37
Q

direct cardiac toxin drugs

A

Ethanol, cocaine, amphetamines and drugs that end in -nib and -mab

38
Q

Name drugs that lead to water retention 1or Na retention

A

NSAIDs, COX-2 inhibitors, androgens, Estrogens, glucocorticoids, rosiglitazone, pioglitazone

39
Q

clinical presentation of HF

A

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
Q

major signs and symptoms of pulmonary congestion

A

exertional dyspnea (DOE)
Orthopnea
paroxysmal nocturnal dyspnea (PND)
bendopnea

41
Q

major signs and symptoms of venous congestion

A

Rales
peripheral edema
hepatojugular reflex
JVD
displacement of PMI

42
Q

Why would an MI cause HF

A

infarct- death of tissue.
scar tissue forms and scar does not contract as well.

43
Q

Why would HTN cause HF

A

increases pressure and heart has to remodel itself

44
Q

activation of SNS results in

A

peripheral vasoconstriction
increased cardiac contractility and HR

45
Q

BNP and NT-pro BNP nortmal levels

A

BNP<35
NT-pro BP<125

46
Q

assessment to diagnose HF

A
  1. clinical history
    physical exam
    ECG, labs
  2. NT pro BNP>125
    BNP>35
  3. transthoracic echocardiogram
47
Q

how to classify HF based of LVEF

A

LVEF<40%- HFrEF
LVEF 41-49- HFmrEF
LVEF>50- HFpEF

48
Q

NYHA classicifaction of HF

A

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
Q

AHA classification of HF

A

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
Q

Simple way to diagnose AHA classes

A

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
Q

Dietary measures for HF

A

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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