| What is cardiogenic shock? | Common cause of mortality with challenging management.
It is caused by severe impairment of myocardial performance resulting in diminished CO, end-organ hypoperfusion and hypoxia.
Clinically presents as hypotension with end-organ hypoperfusion features
Acute MI accounts for 81% of CS |
| What are the characteristics of CS? | Systemic hypoperfusion due to CO depression (Cardiac index <2.2), sustained systolic hypotension despite elevated filling pressure (PCWP>18 mmHg) (SBP <90 for 30 mins)
Evidence of end-organ hypoperfusion (urine output <30ml/h, cool extremities, altered mental status)
In hospital mortality of >50% |
| What are etiologies causing CS? | AMI/ ischemia (LV failure, ventricular septal rupture, papillary muscle ruputure, ventricular free wall rupture, other conditions)
Hemorrhage (infection, excessive vasodilator meds, prior valvular disease, hyperglycemia/ketoacidosis)
Severe valvular disease (AS/MS, aortic regurgitation/ mitral regurg)
Toxic (b-blockers/ calcium channel antagonist overload)
RV failure, bradyarrhythmias (refractory), pericardial tamponade, post-cardiac arrest, post-cardiotomy, cardiomyopathy, takotsubo, hypertrophic cardiomyopathy... |
| How is the epidemiology of CS? | 5-10% of AMI cases will complicate to CS causing death (leading cause of AMI death)
STEMI (ST elevation MI) is associated with 2x risk to get CS than non STEMI (NSTEMI) |
| How is the presentation of CS? | Pt commonly present with cool extremities and signs of pulmonary cogenstion (Cold and wet presentation (reduced cardiac index, increased vascular resistance, and increased PCWP))
Pt may also present Cold and dry (reduced CI, increased resistance but normal PCWP- euvolumic (were exposed to previous MI or CKD))
Wet and warm (also could occur, systemic inflammatory response syndrome in conjugation with MI with higher degree of mortality and sepsis, pt have reduced CI, low-normal vascular resistance, elevated PCWP |
| How is pathophysiology of CS? | . |
| How is typical pt profile in CS? | Old, female, Prior MI, diabetic, anterior MI location, extensive coronary artery stenosis
If it was caused by first inferior MI, we should look for any mechanical cause |
| When is the timing of CS? | 1/4 on admission, 1/4 rapidly after it (within 6h of MI), 1/4 later on first day
Onset may be due to reinfarction, infarct expansion or mechanical complication |
| How is the dx of a CS? | Clinical (dyspnea, paleness, altered mental status, weak rapid pulse, or bradycardia due to high-grade heart block, hypotension with narrow PP, tachypnea, cheyen-stokes respirations, jugular vein distention, oligouria (maybe)
Labs (leukocytosis (left shift), urea and creatinine rise, liver hypoperfusion elevates liver proteins, lactic acid elevated, ABG (hypoxemia and acidosis, maybe compensated by respiratory alkalosis), cardiac markers (CPK, MB, Troponin I and T elevated))
ECG (Anterior infarct (more than half), ST depression (left main stenosis cause), AMI with LV failure (Q wave / ST elevation, LBBB)
CXR (pulmonary vascular congestion and pulmonary edema (only third of pts), normal Heart size (may be enlarged in first MI)
TTE (sees severity and dx (shunts, PE, dissection)
Left heart catheter (may be done)) |
| How is the treatment of CS? | Depends on the clinical signs, tx of arrhythmias.
hypovolemia (administer fluid, transfusion, vasopressors...)
low output CS (check pressure (if HTN ->give nitroglycerin, if normal give dobutamine, if low give NE/dopamine)
acute pulmonary edema (check BP, if high give ACE inhibitors (short acting))
We can also use intraaortic baloon pump/ reperfusion/ revascularization. |
| What is mechanism of fluid accumulation causing pulmonary edema? | Depends on balance of hydrostatic and oncotic pressures of pulmonary capillaries and surrounding tissues.
Hydrostatic favors fluid to move from capillaries to interstitium, oncotic (protein concentration) favors moving to vessels.
Cirrhosis, nephrotic syndrome cause low plasma proteins, causing hydrostatic fluid to go out, in addition, disruption of endothelia will allow proteins to go out of capillaries into tissue causing pulmonary edema (hydrostatic alone isn't enough for edema) |
| What is cardiogenic pulmonary edema? | Cardiac issue, increases pulmonary venous pressure, increases hydrostatic pressure and fluid exits to tissue, and in severe cases causes alveolar edema.
To compromise and comfort breathing we may get pleural effusions |
| What are the clinical manifestations of pulmonary edema? | Rapid onset dyspnea, tachypnea, tachycardia, severe hypoxemia, crackles and wheezes due to alveolar flood and airway compression
Catecholamine release causes HTN
CXR: peribronchial thickening, vascular markings upper zone, kerly B lines, as it worsens: patchy alveolar filling, which progresses into alveolar infiltrates. |
| What is non cardiogenic pulmonary edema? | Due to damage in pulmonary capillaries , leak of proteins and other macromolecules to lung tissues (oncotic pressure)
Associated with dysfunction of surfactant, increase surface forces, alveoli collapse
Intrapulmonary shunt with hypoxemia and decreased pulmonary compliance leading to decreased residual capacity
Normal intracardial pressure should be occurring for Non cardiogenic pulmonary edema |
| What are causes of non-cardiogenic pulmonary edema? | Lung injury (trauma, aspiration, smoke, pneumonia, oxygen toxicity, embolism)
Hematogenous injury (sepsis, pancreatitis, leukoagglutination, multiple transfusions, IV drug use, cardiopulmonary bypass)
Possible lung injury + increased Hydrostatic pressure (high-altitiude, neurogenic, reexpansion edema) |
