Exam 2 lecture 1 Flashcards
What are the two types of HF
Chronic HF
Acute HF
What are the types of chronic HF
Asymptomatic reduced ejection fraction
HFrEF
HFpEF
age related increase in likelihood of HF
60-69 -increases 5%
70-79- increases 7%
80-90- increases 10 %
5 year survival rate of HF
50%
What is the most common hospital discharge for patients >65
HF
definition of HF
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)
Which diseases lead to left ventricular dysfunction
CAD, HTN, cardiomyopathy
What are non-cardiac factors that lead to HF
Endothelial dysfunction, neurohormonal activation, vasoconstriction and Na retention lead to remodelling of the left ventricle, leading to reduction in ejection fraction.
cure for HF
transplant
Two main types of HF
HFrEF
HFpEF
what is HFrEF
Impairment in diastolic dysfunction. leads to reduced contractility.
What is HFpEF
Impairment in diastolic dysfunction, leads to impairement in ventricular relaxation and filling. .
Difference between HFrEF and HFpEF
HFrEF- systolic dysfunction and LVEF<40%
HFpEF- diastolic dysfunction and LVEF>40%
causes of HFrEF
Dilated ventricle
- ischemia dilated CM (70% of cases)
- non-ischemia dilated CM
- cHTN, Thyroid, obesity, stress, cardiotoxins, myocarditis
cause of HFpEF
HTN (most common cause)
What are the 3 determinants of left ventricular performance
Preload
myocardial contractility
afterload
Preload meaning
Venous return; LV end- diastolic volume
myocardial contractility meaning
Force generated at any given LVED
Afterload meaning
Aortic impedance and wall stress
relationship between preload and stroke volume
Increase preload =increase SV
Frank starling curve X and Y axis names
Y- stroke volume
X- LV end diastolic pressure
pressure volume relationship X and Y axis names
Y- SV
X- afterload or SVR
What drugs could reduce preload
diuretics (SGLT2)
HF starts with a reduction in
Cardiac output.
reduced cardiac output in HF has what effect on the body
leads to a reduction in BP and organ perfusion.
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
What do SNS, RAAS and vasopressin lead to
arrythmias, cell death and CM hypertrophy
Why would arrythmias happen with SNS
`catecholamines are released when SNS is activated. This pre disposes pts to arrythmias
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
How does RAAS, SNS and vasopressin increase affect BP and HR
increases them
what are the compensatory responses to HF
- increase in preload due to Na/H20 retention
- Vasoconstriction
- Tachycardia and increase in contractility (SNSactivation)
- ventricular hypertrophy and remodelling
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
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
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
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
factors percipitating or worsening HF
lack of compliance with drug or diet
uncontrolled HTN
cardiac arrythmia
A- fib
Atrial flutter
are B blockers positive or negative ionotropes?
verapamil? Diltiazem?
negative (reduce contractility)
verapamil and diltiazem are also negative ionotropes
Name negative ionotropic drugs
Antiarrythmics (disopyramide, felcanide)
B blockers
non DHP CCB
itraconazole
direct cardiac toxin drugs
Ethanol, cocaine, amphetamines and drugs that end in -nib and -mab
Name drugs that lead to water retention 1or Na retention
NSAIDs, COX-2 inhibitors, androgens, Estrogens, glucocorticoids, rosiglitazone, pioglitazone
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
major signs and symptoms of pulmonary congestion
exertional dyspnea (DOE)
Orthopnea
paroxysmal nocturnal dyspnea (PND)
bendopnea
major signs and symptoms of venous congestion
Rales
peripheral edema
hepatojugular reflex
JVD
displacement of PMI
Why would an MI cause HF
infarct- death of tissue.
scar tissue forms and scar does not contract as well.
Why would HTN cause HF
increases pressure and heart has to remodel itself
activation of SNS results in
peripheral vasoconstriction
increased cardiac contractility and HR
BNP and NT-pro BNP nortmal levels
BNP<35
NT-pro BP<125
assessment to diagnose HF
- clinical history
physical exam
ECG, labs - NT pro BNP>125
BNP>35 - transthoracic echocardiogram
how to classify HF based of LVEF
LVEF<40%- HFrEF
LVEF 41-49- HFmrEF
LVEF>50- HFpEF
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
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)
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)
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
