HY lecture notes:
How does isolated left heart failure present? → fluid in the lungs (pulmonary edema) +/- pleural effusion; orthopnea, paroxysmal nocturnal dyspnea (PND); depending on the etiology of the heart failure, the structure of the heart will take on different characteristics, but the important point about LH failure is fluid in the lungs → also really important you know that pulmonary capillary wedge pressure (PCWP) is increased in any LH pathology (even if the pressure is within the acceptable range prior to full-blown LH decompensation, the PCWP is still increased relative to the patient’s original baseline in LH pathology.
What is PCWP? → equal to left atrial pressure; if you stick a catheter through the venous circulation all the way back to the right heart, and then into the pulmonary circulation, and then into a distal pulmonary capillary such that it can’t go any farther, the pressure reverberations are said to best reflect those of the left atrium. The USMLE is obsessed with PCWP; you need to know it is increased not just in cardiogenic shock, but also in LH pathology as I’ve stated above.
High PCWP occurs if there is any left heart pathology. Not just in cardiogenic shock, but also in mitral stenosis (increased afterload on LA → so more pressure in LA → higher PCWP) or mitral regurg (higher preload in LA → higher pressure → higher PCWP), as well as any cause of left ventricular hypertrophy (if the LV is experiencing a pressure or volume overload, that effect will back up to the LA).
In aortic stenosis → higher afterload on LV (concentric hypertrophy) → therefore higher afterload on LA → higher PCWP.
In aortic regurg → higher preload on LV (eccentric hypertrophy) → therefore higher preload on LA → higher PCWP.
It should also be noted that it is very rarely stated that the left atrium “hypertrophies”; the LV will hypertrophy; the LA will dilate. Any pathology at the level of the mitral valve or later (LV, aortic valve, or aorta) will cause left atrial dilatation and increased PCWP.
Most pleural effusions are due to either congestive heart failure (CHF) or malignancy.
CHF = left heart failure + right heart failure.
The most common cause of right heart failure is left heart failure.
Therefore in CHF, PCWP is high → this increased pulmonary pressure leads to pulmonary hypertension (where there is actual hypertrophy of the tunica media of the pulmonary arteries) → backs up to the RV → right heart failure.
So let’s say you’ve got fluid in the lungs, but they say PCWP is normal → that means the fluid in the lungs can’t be due to left-heart origin because, if it were, PCWP would have to be high.
ARDS (acute respiratory distress syndrome) presents with normal PCWP. ARDS is when proteinaceous fluid leaks out into the alveoli bilaterally and is frequently due to sepsis, trauma, or pancreatitis. So USMLE Qs like to say, e.g., 50M alcoholic with abdo pain gets dyspnea with bilateral infiltrates + his PCWP is normal → Dx = ARDS.
In ARDS, pO2/FiO2 must be less than 300. It is treated with low-tidal-volume mechanical ventilation (prevents barotrauma) + permissive hypercapnia (we allow CO2 to be slightly elevated [>44 mmHg] to prevent barotrauma).
For cor pulmonale, probably the most important piece of info regarding this condition is that PCWP is normal, which tells you the cause of the RH failure cannot be from LH origin. For instance, if you have a guy with COPD who also has heart disease, if his PCWP is elevated, then we cannot conclude that his right heart failure is a result of the lung disease in isolation because increased PCWP can lead to RH failure.
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Hypovolemic shock: low VR, low CO, high TPR, low PCWP
Distributive shock (anaphylactic, septic, neurogenic): high VR, high CO, low TPR, normal PCWP
Cardiogenic shock: low VR, low CO, high TPR, high PCWP
