Hypotension SOB, Heart Failure (Quiz 2) Flashcards
Heart failure & cardiogenic shock is defined as?
—A potentially life threatening condition where the heart is unable to pump sufficiently to supply oxygen-rich blood to meet the metabolic demands of the other organs in the body.
—➡️ inadequate tissue perfusion, end organ damage, and multi-system failure.
—Heart Failure may be the final manifestation of every form of other cardiac disease
—Cardiogenic shock carries a 40-70% mortality.
Heart failure types
What is it relating to
How is it categorised nowadays
IMPAIR VENTRICULAR CONTRACTILITY
or
IMPAIR VENTRICULAR RELAXATION OR FILLING
—Systolic Heart Failure: impaired contractility
—Diastolic Heart Failure: impaired filling
There is overlap between the two processes therefore more common to define heart failure now as:
1️⃣ Heart Failure with reduced EF (<40%)
2️⃣ Heart Failure with preserved EF (>40%)
Normal EF is 55-60%
—amount of blood ejected from the left ventricle with each heartbeat
HF w/ reduced EF — why does the ventricle have diminished capacity to eject blood? 3
What are some causes?
The ventricle has a diminished capacity to eject blood due to:
1️⃣ Impaired myocardial contractility d/t destruction of myocytes, abnormal myocyte function, or fibrosis
2️⃣ Pressure overload (excessive afterload) — impairs the LV by increasing resistance to flow (HTN)
3️⃣ coronary artery disease
OTHER CAUSES relate to disease processes that affect:
—cardiac myocardium (MI, myocarditis, drugs)
—aorta (hypertension)
—valves
—electrical system (tachyarrhythmias)
—as well as congenital heart disease.
—rheumatologic systemic disease
—endocrine disorders
—pregnancy (peripartum cardiomyopathy)
—stress (takotsubo)
HF w/ preserved EF (HFpEF)
What are the two broad causes? What are THEY causes by ?
Abnormalities with one of the following or BOTH:
1️⃣ Impaired early diastolic relaxation (energy dependent process)
—Diastolic early relaxation is usually related to a MI
2️⃣ Increased stiffness of the LV
—Left ventricular hypertrophy, fibrosis, or restrictive cardiomyopathy typically cause the LV to be chronically stiff
—Pericardial constriction and tamponade call also cause forms of diastolic dysfunction
Classic patient is older woman
Right sided HF
What is the right ventricle susceptible to?
Common cause of r.sided HF?
Isolated r.sided HF results from?
—right ventricle is thin walled but highly compliant to accepting blood volume.
—susceptible to failure in situations that suddenly increase afterload
The MOST COMMON CAUSE of right sided HF is left sided heart failure.
Isolated right sided HF results from:
—pulmonary diseases aka COR PULMONALE d/t increased pulmonary artery pressures.
PULMONARY PARENCHYMAL DISEASE
—COPD
—interstitial lung disease
—bronchiectasis
PULMONARY VASCULAR DISEASE
—pulmonary embolism
—primary pulmonary hypertension
What are the compensatory mechanisms that activate in systolic HF? (HFrEF/Low EF) — 3
memorise the equation in the image
Three mechanisms help counter the drop in cardiac output and preserve sufficient blood pressure to perfuse vital organs:
-
Frank-Starling Mechanism
—With decreased CO, in a healthy heart, more blood comes in, more stretch, better snap/squeeze. Dehydration would be one reason for low SV. Increases pre-load. In a failing heart, this mechanism doesn‘t work. -
Neurohormonal Alterations notice decrease BP and activate:
—Adrenergic nervous system
—Renin-angiotensin-aldosterone system (RAAS)
—Increased antidiuretic hormone (ADH/vasopressin)
causing more water retention, more vasoconstriction. These benefit at first but are detrimental in the long run
-
Ventricular Hypertrophy and Remodeling
—to increase contractility but it will fail over time
—it makes the muscle stiff
Frank-Starling
What is the mechanism here?
Stretch versus Snap = the greater the stretch, the more forceful the snap
In a failing heart however, the contractility (snap) is impaired.
Therefore more diastolic filling (stretch) results in a lower stroke volume than normal.
The residual volume induces a greater stretch on the myofibers in the subsequent beat, which helps empty the LV and preserve cardiac output.
This compensatory mechanism will eventually fail and the subsequent volume will go retrograde into the lower pressure left atrium and pulmonary pressures.
Neurohormonal alterations
Activate in response to low cardiac output is to increase SYSTEMIC VASCULAR RESISTANCE which helps maintain arterial perfusion to vital organs
BP = CO x TPR
if cardiac output is low, increase TPR to increase BP to perfuse organs
Also increase salt and water retention which INCREASES INTRAVASCULAR VOLUME and LV PRELOAD, maximizing stroke volume via the Frank-Starling mechanism.
Beneficial acutely to preserve cardiac output however chronic activation of these mechanisms are devastating to the failing heart and contribute to a decline in cardiac output.
Harmful effects
—Increased volume and augmented venous return to the heart WORSEN congestive pulmonary systems
—Elevated arteriolar resistance INCREASES the load which the failing LV has to contract against DECREASING stroke volume and cardiac output
—Increased heart rate increases metabolic demand and reduced the performance of the left ventricle
—Continuous SYMPATHETIC activation results in DOWN REGULATION of B adrenergic receptors DECREASING the myocardium’s sensitivity to circulating catecholamines and REDUCED inotropic response
—Chronically elevated levels of AII (angiotensin II) and Aldosterone increase production of cytokines, activate macrophages, stimulate fibroblasts, and lead to FIBROSIS and ADVERSE/NEGATIVE REMODELING of the failing left ventricle
Beneficial neurohormonal alteration
Which peptides are released?
What is their effect?
NATRIURETIC PEPTIDES are natural hormones secreted in heart failure (congested & stressed) in response to INCREASED intracardiac pressures:
1️⃣ ANP or atrial natriuretic peptide released with atrial dilation
2️⃣ BNP B-type or brain natriuretic peptide is released when the ventricular myocardium is subject to hemodynamic stress or increased radius or pressure
—proBNP is a prohormone that generates both BNP and an inert N-terminal proBNP
RESULT is the EXCRETION of sodium and water, VASODILATION, INHIBITION of renin, and antagonize the effects of AII on aldosterone and vasopressin
Problem = they are INSUFFICIENT to counteract the effects of the other activated neurohormonal systems. True benefit is diagnostic but they can‘t really overcome the neurohormal systems
Ventricular hypertrophy & remodeling
1️⃣ LV Wall Stress increases due to chamber dilation or the need for greater pressure to overcome increased afterload
2️⃣ Myocardial Hypertrophy results to counter the effect of increased wall stress and maintain contractile force ➡️ increased LV stiffness & elevated diastolic pressures which then transmit retrograde
—Chronic volume overload leads to chamber dilation ➡️ new sarcomeres form in series with the old ones causing ELONGATION of myocytes and ECCENTRIC HYPERTROPHY
—Chronic pressure overload leads to the synthesis of new sarcomeres in parallel with the old ones causing THICKENING of the myocytes and CONCENTRIC HYPERTROPHY
3️⃣ Ultimately ventricular function will decline allowing the chamber to dilate out of proportion to wall thickness
Precipitating factors of HF
What factors tip a patient into decompensation? 6
—pts may be asymptomatic for extended periods of time because of either mild impairment or the result of the compensatory mechanisms.
Events that increase cardiac workload can tip them into DECOMPENSATION:
1️⃣ Increased Metabolic Demands:
—fever, infection, anemia, tachycardia, hypothyroidism, pregnancy
2️⃣ Increased Volume:
—excessive dietary sodium or fluids
—renal failure (pt misses dialysis)
3️⃣ Increased Afterload:
—uncontrolled hypertension, PE
4️⃣ Impaired Contractility:
—MI, drug induced (alcohol), negative inotropic agents
5️⃣ Failure to take prescribed medications
—in an exacerbation, if mildly congested, half their BB, if they‘re severe, hold the BB until they‘re euvolemic and then titration back up
6️⃣ Excessively slow heart rate
What are the signs and symptoms of HF?
—Dyspnea (on exertion) and Orthopnea
—Paroxysmal Nocturnal Dyspnea (resorption of edema)
—Cheyne-Stokes Respiratory Pattern (advanced HF, tachypnea then period of apnea, then again)
—Fatigue and Confusion (low CO for cerebral perfusion)
—Palpitations
—Syncope
—Abdominal Pain/Nausea/Early Satiety (Ascites)
—Cool/Mottled Skin (low SV/CO, entering cardiogenic shock)
—Edema/Weight Gain
—Elevated JVD
—Ascites/Hepatomegaly (right sided HF, backs up into portal venous system. RUQ pain)
—S3 Gallop and Mitral/Tricuspid Regurgitation
—Tachycardia
—Hypotension
—Pulsus Alterans (one strong beat, followed by a weak beat)
—Decreased Urinary Output (kidneys not getting perfused, CO decrease, entering cardiogenic shock)
What could cause:
—warm and dry
—warm and wet
—cold and dry
—cold and wet
Systolic HF:
—warm and dry: normal
—warm and wet: most patients, not in shock, have HF, EF down, holding on to a lot of edema but still perfusing organs. Diurese and afterload reduce them
—cold and dry: cardiogenic shock
—cold and wet: cardiogenic shock, low output, not perfusing. Congested. Diurese these patients.
HF diagnostics — what do these tell you?
BMP
LFTs
CBC
BNP ⭐️ [know this]
Cardiac Enzymes
TSH
Drug Screen
Iron Studies
Lactate / VBG (pH)
EKG
Chest Radiograph
Echo
Coronary Angiography
BMP
—Hyponatremia = poor prognostic sign. HF patients are usually hypervolemic hyponatremic. They are congested
—Elevated BUN and Creatinine (cardiorenal syndrome/pre-renal = heart not perfusing kidney) with Hyperkalemia
—Hypokalemia and Hypomagnesemia = arrhythmia risk
LFTs
—Transaminitis from hepatic congestion or shock liver
CBC
—Anemia a/w increased mortality
BNP ⭐️
—Released in setting of increased ventricular dilation or wall stress (HF). Elevated
Cardiac Enzymes
—Rule out acute MI versus supply demand ischemia
TSH
Drug Screen
Iron Studies
—could be diastolic HF
—hemachromatosis
Lactate / VBG (pH)
—make sure not in lactic acidosis
EKG
—Presence of Q waves to indicate prior MI or acute ST segment changes for ongoing ischemia/injury
—Chamber enlargement:
—Hypertrophy or Low Voltage
—Conduction Disease (LBBB suggesting dyssynchrony)
—Atrial Arrhythmias
Chest Radiograph
—Heart Size
—Pulmonary Edema
—Pleural Effusions
—Rule Out Infection
—Lines
Echo — tells us the EF
—Most useful diagnostic test as provides extensive information about the structural condition of the heart allowing one to determine the etiology of heart failure/shock.
—Convenient and harmless study
—Evaluate for regional wall motion abnormality in setting of a coronary artery distribution to indicate ischemia
—Valvular Disease
—Non-ischemic Dilated Cardiomyopathy
Coronary Angiography
—Important to define the coronary anatomy to help determine etiology of heart failure
—If acute, early revascularization in patients with a myocardial infarction and shock has proved to have a mortality benefit in patients < 75 years of age and absence of contraindications.
—Ischemic disease is the number one cause of systolic HF
Diagnositics for shock
Right Heart Catheterization
—Pulmonary capillary wedge pressure (PCWP) > 15 mmHg
—Central venous pressure > 10 mmHg
—Decreased mixed venous oxygen saturation
—Cardiac index < 2.2 L/min/kg/m2
Systolic blood pressure < 90 mmHg for at least 30 minutes
generally reserved for very sick patients in the ICU
HF with Reduced EF - Management
Need to differentiate Acute and Chronic Management
If acute, determine if:
—cold and wet (shock)
—cold and dry (low output/shock)
—warm and wet (decompensated)
Management Strategy Guideline: [know]
—Preload
—Pump
—Afterload
—Devices
What are the two paradigms to cardiogenic shock?
1️⃣ A drop in cardiac output resulting in hypotension, tachycardia, and compensatory increase in vasoconstriction/systemic vascular resistance to maintain tissue perfusion. Along spectrum of progression of systolic heart failure.
2️⃣ Acute drop in cardiac output causing SIRS like response with drop in systemic resistance similar to septic shock (20%).
Treatment of shock
6
Inotropic Agents
—support a failing left ventricle (mechanical and electrical)
—see table of medications
—milrinone, dobutamine, dopamine frequently used
Vasodilators
—preload and afterload reduction
Vasopressors
—may be needed to maintain an effective mean arterial pressure
—if MAP is 45, you want 60, so might need to clamp down on BP to get organ perfusion
Diuretics
Ultrafiltration
—like dialysis to get volume off
Oxygen support / Noninvasive Positive Pressure Ventilation
Treatment of shock
What are the additional adjunctive hemodynamic support therapies?
Intra-aortic balloon pump IABP
Percutaneous ventricular assist devices
1️⃣ Mechanical support from an Intra-aortic Balloon Pump (IABP): Reduces afterload, improves cardiac output, and augments diastole which improves coronary perfusion
2️⃣ Percutaneous Ventricular Assist Devices including the Tandem Heart and Impella. They can bridge to recovery or more definitive therapy. The TandemHeart provides left atrial to femoral artery bypass flow at rates up to 5 L/min. The Impella is an intracardiac ventricular flow device that can provide 2.5 to 5 L/min support.
Treatment of shock
What are the additional adjunctive hemodynamic support therapies?
ECMO
LVAD
3️⃣ Extracorporeal Membrane Oxygenation (ECMO): Life support machine replacing the function of both the heart and lungs. The machine removes blood from the patient to an oxygenator which removes carbon dioxide and adds oxygen. The blood is then returned to the patient via a pump that circulates it through the body replacing the function of the heart.
4️⃣ Left Ventricular Assist Device (LVAD): Mechanical pump surgically implanted in patients to circulate blood while a patient awaits a transplant. One end of the pump is attached to the left ventricle and the other attaches to the aorta.
What are the five alive? (Or 4)
ACE, ARB or ARNI
BB
MRA (Aldo antagonist)
SGLT2 inhibitor
so really only 4
