CHF Flashcards
1 cause of left heart failure and right heart failure
L: MI
R: PE
What are the 3 determinants of stroke volume
- preload
- afterload
- myocardial contractility
CO=SV x HR
The amount of myocardial stretch at the end of diastole
Preload
*The more a normal ventricle is distended (filled with blood) during diastole, the greater the volume of blood ejected during the next systolic contraction
The resistance a heart must overcome to empty it’s content
afterload
ventricular wall stress increases in response to
- the arterial systolic pressure (i.e. hypertension)
2. Increased chamber size (e.g. dilated heart chamber)
___ serves an initial compensatory role in reducing wall stress
An increase in wall thickness
changes in the force generated by the myocardium for a given set of preload and afterload conditions
contractility
3 causes of heart failure
(decreased Cardiac Output)
- Impaired ventricular filling (Decrease in Preload)
- Increased Afterload
- Impaired Contractility
What happens to preload, afterload, and contractility as SV increases
- Increase in preload
- Decrease in afterload
- Increased contractility
What type of heart failure is more common
systolic (2/3)- Ventricles become enlarged, and pump out less than 40-50% of blood
Cause of diastolic dysfunction and systolic dysfunction
Diastolic: Decreased filling
Ventricles stiff/cannot relax
Normal left ventricular ejection fraction (> 50%)
-CO limited during exertion (cannot take in larger volume in ventricle)
Systolic: Cause: Impaired Contractility or excessive afterload
Ventricles thinned, stretched, enlarged
Decreased LVEF (<40-50%)
-decreased output
Causes of Left sided HF
- MI (#1 cause)
- Aortic stenosis
- uncontrolled HTN
- Mitral stenosis
- percaridal tamponade
- LVH
- dilated cardiomyopathy
(change this card)
__ Ventricle is thinner / highly compliant as it ejects against a low pulmonary vascular resistance.
Right
*Very susceptible with sudden increases in afterload (e.g. PE)
isolated right heart failure is care (called __)
cor pulmonale
Most common cause of right heart failure is
left heart failure
Presentation of left sided heart failure
- Dyspnea,
- Orthopnea,
- Paroxysmal Nocturnal Dyspnea,
- Nocturnal Cough
*Back up comes from lungs therefore lung sx
Presentation of right sided heart failure
- Peripheral Edema,
- RUQ Discomfort / hepatic enlargement
*Back up comes from body therefore sx in body
Describe the cycle of chronic HF
- increased BP/CO
- increased cardiac workload
- LV dysfunction
- Decreased CO/BP
- hemodynamic remodeling, neurohormonal activation
- increased HR, contractility, vasoconstriction, increased volume
* cycle continues
Compensatory mechanism of HF
- ALL in response to decreased BP (BP = CO x TPR)
- Neurohormonal mechanisms (increase TPR)
- Autocrine System of Myocytes (Natriuretic Peptides)
- Ventricular Hypertrophy and Remodeling
*These are targets for treatment!!
Neurohormonal mechanisms (increase TPR)
- Sympathetic Nervous System (Adrenergic mechanisms)
- RAA system
- Increased ADH
How does the sympathetic nervous system compensate in HF
- Decreased CO = Decreased Perfusion pressure to baroreceptors in the heart (low BP)
- Sympathetic and Adrenal Epi / Norepi outflow to the heart and peripheral circulation is increased
-Increased CO: Increased heart rate (B-adrenergic stim.)
contractility
-Increased TPR: Vasoconstriction 2/2 alpha receptors
*Excess norepinephrine “toxic” to myocyte
Excess ___ “toxic” to myocyte
norepinephrine
RAA/ADH system response to HF and its effects
- Decreased CO = Decreased Perfusion pressure to juxtaglomerular cells / macula densa of the kidney
- Increased Renin Release
- Increased ADH (Vasopressin)
EFFECTS: cardiac hypertrophy, vasoconstriction, increase BV, fluid/Na retention,)
___ Lends support to a suspected diagnosis of HF but should not be used in isolation to confirm or exclude the presence of HF.
Elevated BNP
ANP/BNP produced and stored by __. Released in response to ___, __, and ___stimulation
myocytes
atrial/ventricular distension (stretch), Angiotensin II and NE
Elevated BNP is associated with
- hypervolemic states (e.g. HF)
- reduced LVEF
- LVH
- elevated LV filling
- AMI
- PE
- COPD
BNP have a __ and ___ effect
Natriuretic and vasodilatory effect
____ stimulates the development of myocardial hypertrophy and deposition of extracellular matrix which maintains contractile force
A sustained increase in wall stress
Comes at the expense of higher Diastolic ventricular pressures which are transmitted to the left atria and pulmonary vasculature
LVH and remodeling
CHF patients present in 1 of 3 ways:
- Decreased Exercise Tolerance (Fatigue)
- Syndrome of Fluid Retention
- NO symptoms- (i.e. incidental discovery found to have cardiac enlargement or dysfunction)
PE findings of right sided HF
- JVD
- Hepatomegaly
- Peripheral Edema
PE findings of left sided HF
1. Tachycardia, 2,Tachypnea, dyspnea, 3. orthopnea, PND 4. Pulmonary Rales (Crackles) = Fluid at the Alveolar Level 5. Pneumonia or CHF S3 Gallop
Echo (the main tool of HF) ask 3 basic questions
- Is the LVEF preserved or reduced? (55-75%)
- Is the structure of the LV normal or abnormal? (Size, Wall Thickness, and Motion)
- Are there other structural abnormalities (such as valvular, Pericardial, Or right ventricular abnormalities) that could explain the clinical presentation?
- Baseline for comparison
- Severity of structural remodeling
- Repeat assessment of LVEF may be helpful with a major change in clinical status.
EKG changes with heart failure
- LBBB
- LVH
- Afib w/ RVR (140)
*look for evidence of prior MI, LVH, cardiac conduction abnormality or cardiac arrhythmia
Labs to check with heart failure
- Electrolytes
- Renal Function
- CBC
- UA
- A1C
- Lipid Panel
- Hepatic Function
- Thyroid Function
- Transferretin
- HIV
- BNP
*Don’t get all of these all the time be get what is applicable for DDX
Imaging for CHF
- Echo
- EKG
- CXR
- +/- cardiac cath if angina suspected
CXR changes with HF
- What are you looking for:
the degree of cardiac enlargement and pulmonary congestion or to detect the presence of pulmonary disease - cardiomegaly with diffuse pulmonary infiltrate consistent with pulmonary edema.
Risk factors for heart failure
(all can cause remodelling)
- HTN
- Valvular Heart Disease
- Diabetes
- Myocardial infarction
- Atherosclerosis
- Cardiomyopathy
- Arrhythmias and LBBB
- COPD
- Cardiotoxic drugs (smoking, alcohol, cocaine, ephedra, NSAIDs)
Three Classes of drugs can exacerbate the syndrome of HF and should be avoided:
- Antiarrhythmic agents
- CCB’s (vasodilation and worsening edema)
- NSAID’s (Na retention, peripheral vasoconstriction)
Pharmacologic therapy for stage A/B heart failure
- ACEI/ARB (inhibit remodeling)**
2. BBs
Describe the use of BB for HF
- Counters effect of SNS
- Must if post MI (inhibits remodeling)
- Atenolol / Metoprolol (Beta-1 selective)
- Carvedilol (non-selective, but can decrease remodeling) and Labetolol (potent Vasodilator) Can Exacerbate HF
- Start Low, Go Slow to prevent CHF sx
When do you get an Echo for CHF
change of symptoms or exacerbation
Describe the stages of HF
A: at high risk for HF but w/o structural heart dz or sx of HF
B: structural heart disease but w/o signs or sx of HF
C: structural heart dz w/ prior or current sx of HF
D: refractory HF requiring specialized interventions
What stage of HF?
pts w/ known structural heart dz and SOB and fatigue, reduced exercise tolerance
C
What stage of HF?
Pts w/ HTN, atherosclerotic dz, DM, obesity, metaboilc sydnrome or using cardiotoxins w/ FHx CM
A
What stage of HF?
pts w/ previous MI, LV remodeling including LVH and low EF, asymptomatic valve dz
B
What stage of HF?
pt who have marked sx at rest despite maximal therapy (those who are recurrently hospitalized or cannot be safely discharged from hospital w/o specialized intervention
D
Goals of Stage A HF tx
- tx HTN,
- smoking sessation,
- lipids,
- exercise,
- discourage alcohol and ilicit drug use
- control metabolic syndrome
Goals of Stage B HF
- all measures under stage A
Goals of Stage C HF
- all measures under stage A and B
2. dietary salt restriction
Pharmacologic therapy for Stage C/D
- ACEI/ ARBs
- BB
- Diuretics (HCTZ, aldosterone blockers- spironolactone)
- +/- digoxin
*You should really have specialty support at these stages
pharmacological effects of digoxin
- positive inotropic effect (use in Afib)
2. neurohormonal effects (dec. renin and NE at low doses)
When do refer with CHF
- Stage C
- Conduction abnormality
- Suspect prior/unknown MI
- Suspect CAD
- Evidence of PHTN
Non-pharmacologic therapies of HF
- Implantable Cardioverter / Defibrillator
- Non ischemic cardiomyopathy
- LVEF <35% - Tx of arrhythimas (QRS over 0.12s)/ cardiac resynchronization
- revascularization for ischemia
- acute pulmonary edema tx
- LMNOP (Lasix, Morphine, Nitrates (pressors), Oxygen, Position)
Home monitoring of HF goals
Preventing Acute exacerbations / Hospitalizations and Improving QUALITY of life
Home monitoring of HF includes educating about
- Recognition of warning signs of worsening function
- Weight should be monitored daily
- Understanding of Med Regimens
- Diet Adjustment- Salt / sodium Restriction (less than 2000mg QD)
- Promote Moderate Physical Activity if tolerated
- Infections: Pneumo Vax / Influenza Vaccination
*teach pts and family members
Early treatment in HF is important because
slow progression or reverse staging
- HF is progressive and dynamic
- Mortality rates not changing but quality of life can be improved
