Cardiac Flashcards
(17 cards)
What are the differences between systolic and diastolic heart failures?
Systolic is also known as HFrEF or HF with reduced ejection fraction.
* reduced LC contractility (pumping problem)
* large, dilated, congested and overloaded ventricle
* reduced CO (EF <40%), increased preload and increased afterload - inodilators may help here
* S3 sounds
* poorer prognosis
Diastolic is also known as HFpEF or HF with preserved ejection fraction.
* reduced LV filling (stiff ventricle)
* EF stays over 50%
* increased volume/pressure in LA and pulmonary vasculature
* S4 sounds
* more common in women
Signs of cardiogenic shock
When assessing, consider whether this is a mechanical, pump or electrical problem. This is primarily a disorder of cardiac function resulting in an inability to deliver O2 to end organs.
- SBP equal to or under 90, or output equal to or less than 2.2L/min
- PCWP >15 mmHg
- Elevated lactate >4 mmol/L can be a significant sign
- SVO2 <60% (indicates increased extraction due to slow moving blood through the body
- Elevated BNP >100pg/mL
Anterior MI is the highest risk for developing acute onset cardiogenic shock.
What is cardiac remodeling?
Remodeling is a response to increased hemodynamic load and/or neurohormonal activation.
In concentric remodeling, the chamber size is reduced with increasing wall thickness. A response to pressure overload.
In ecentric remodeling, the chamber size increases with a relative decrease in wall thickness. A response to volume overload.
What are the neurohormonal responses to heart failure?
SNS stimulation is activated by baroreceptors to increase catecholamines causing vasoconstruction and increased HR. Increased arrhythmia risk.
RAAS responds to reduced kidney perfusion to vasoconstrict, increase BP and afterload, and increase Na+ and H2O retention.
Ventricular remodeling is a direct cardiac myocyte response to the above, causing hypertrophy and/or chamber enlargement and thinning walls. The new myocytes laid down don’t contract as efficiently and the increased size increases MVO2 demand.
What are the Forrester Classes of HF?
- Warm & dry: cardiac index is over 2.2 L/min and PCWP is less than 18. There may be increased CO in this initial stage.
- Warm & wet: cardiac index is still preserved, however PCWP is rising with signs of fluid retention. Diuretics may be indicated.
- Cold & dry: decrease in cardiac index < 2.2L/min; however, PCWP still under 18 mmHg. Consider inotropes to improve output.
- Cold & wet: decrease in cardiac index and increase in PCWP over 18mmHg. This patient will require vasopressors, inotropes and likely a ventricular assist device.
SCAI stages
Used to categorize the level of cardiogenic shock.
* A at risk: risk factors are present, but no symptoms
* B beginning: relative hypotension or tachycardia, but no hypoperfusion
* C classic: pt requires inotropes, vasopressors or mechanical support
* D deteriorating: unable to stabilize with above treatments
* E extremis: circulatory collapse, cardiac arrest, needs ECMO or transplant
What can we use to manipulate cardiac output?
As a function of HR x Stroke Volume
Heart rate can be increased with beta agonists, or decreased with beta blockers.
Stroke volume
* Preload is increased with fluids, and decreased with diuretics and venodilators.
* Afterload is increased with vasoconstrictors, and decreased with arterial venodilators.
* Contractility is increased with positive inotropes, and decreased with beta blockers and calcium channel blockers.
What are the 3 v’s of afterload factors?
- Vessel diameter (vasoconstriction, vasodilation)
- Valve (is there stenosis)
- Viscosity (measured by hematocrit)
Diastolic pressure is an indicator of arterial tone. Reducing afterload may increase CO.
Briefly describe the NYHA, CCS and Killip scores
NYHA categorizes functional limitations of patients with HF based on fatigue/SOB.
CCS evaluates the severity of angina based on activity levels inducing chest pain and degree of limitation it causes.
Killip asesses the severity of heart failure in patients experiencing acute MI. Looks at S3, pulmonary edema and JVP as well as Forrester Class 4 signs of shock.
What are factors affecting contractility?
- MI, failure, cardiomyopathies
- High afterload is harder to push against
- SNS response
- Electrolyte imbalances, particularly Ca++
- Tachycardia (less filling time)
- aFib
- Medications (BB/CCB)
- Low preload
What is pulsus paradoxus, and what causes it?
Exaggerated drop in SBP (>10 mmHg)during inspiration. Causes involve compression or changes in interthoracic pressure. I.e. tamponade, constrictive pericarditis, severe asthma/COPD, PE, tension pneumo, RV infarction, and restrictive cardiomyopathy.
AAA Description
AAA is a full thickness dilation of the vessel, and is considered clinically relevant when it’s over 50% of the vessel diameter. Most people have 2cm vessels, so over 3cm is considered aneurysmal, and surgery is performed when the aneurysm is >5.5cm.
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* 65% are infrarenal below renal arteries
* 35% are suprarenal
How does mecanical ventilation affect the RV?
Pros
Improving gas exchange will reduce hypoxic pulmonary vasoconstriction, decreasing RV afterload.
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Cons
* decreased RV return (preload)
* some increase in pulmonary hypertension due to increased intrathoracic pressure
* if CO decreases, RV may dilate and cause a left shift in the septum
* compensatory increase in SVR due to reduced RV output
How does mechanical ventilation affect the LV?
Pros
* decreased afterload, and less dilation - may help reduce any mitral regurgitation by closing gaps
* Increased pressure gradient from thorax to periphery helps with flos
* decreased wall stress, reducing MVO2
* hydrostatic displacement of alveolar edema supports preload
Cons
* decreased preload from reduced RV output
* decreased stroke volume due to interventricular dependence (if RV is overloaded)
Describe patho and treatment goals for stenotic LV valves.
Mitral
Valvular inflammation most commonly caused by rheumatic fever hx. Prevents LA emptying into LV, so LA becomes overloaded easily and backup can seep into the lungs.
Tx goal: optimize filling time, HR goal is 70-80bpm, managed through BB/CCB’s, digoxin.
Aortic
Often atherosclerotic factors stiffen the valve, preventing forward flow during systole, and causing LV hypertrophy.
Tx goals: careful treatment of hypertension, reduce afterload to improve pressure gradient on either side of the stenotic valve. Intubation is highly risky because of intolerance to brief afterload increases or HR changes.
Describe patho and treatment goals for regurgitant LV valves.
Mitral
Chordae, leaflet, annulus or valvulare disruption causes blood to flow backwards into LA during systole.
Tx goals: reduce afterload so pressure gradient encourages flow into the aorta. Nitroprusside is agent of choice: 1.5-10mcg/kg/min
Aortic
Dilation of ascending aorta causes backward flow of blood from aorta to LV during diastole.
Tx goals: avoid ANY reduction in HR to continually maintain forward flow (no BB’s or CCB’s)
3 Post MI Mechanical complications
These should be considered in any acute MI patient with new murmer, hypoperfusion, decompensated HF or cardiogenic shock.
- LV wall rupture leads to hemipericardium, temponade then PEA. Treatment is pericardiocenticis, fluids, inotropes and vasopressors.
- Septal wall rupture presents with a new murmer, dyspnea, cardiogenic shock. Treatment is inotropes and vasopressors.
- Papillary muscle rupture presents with hypotension and severe pulmonary edema +/- new murmer. Treatment focus is afterload reduction, diuretics, vasopressors and intraaortic balloon.
