Cardiovascular: USMLE Step 1 video lessons
Cardiac physiology, the pressure-volume loop, haemodynamics and the heart in disease.
The left ventricular pressure–volume loop, built corner by corner, then pushed by preload, afterload and contractility so you can predict how each one reshapes the loop.
5:00Pressure-volume loop explained: four phases, four valve events
One heartbeat drawn as a single shape. Learn which corner of the pressure-volume loop is which valve, which way the loop runs, and how to read stroke volume and ejection fraction straight off it.
5:04Preload on the pressure-volume loop: EDV, stroke volume and the EDPVR
Give fluid or lose blood, and the same heart draws a different loop. See how preload slides one corner of the pressure-volume loop, and why the other side barely moves.
4:49Afterload on the pressure-volume loop
Afterload on the pressure-volume loop is a line, not a number. Pivot it and the end-systolic point slides along a fixed ESPVR: higher afterload means a taller, narrower loop and less blood out.
5:17Contractility on the pressure-volume loop: the ESPVR explained
Contractility on the pressure-volume loop shows up as the slope of the ESPVR. More contractility steepens it, so ejection runs to a smaller volume; less contractility flattens it.
5:30Wiggers diagram explained: the cardiac cycle step by step
A Wiggers diagram is a few traces on one time axis. One rule decodes it: blood moves down a pressure gradient, and each valve is a one-way door that obeys the gradient.
4:44The Frank-Starling curve: preload, inotropy and heart failure
The Frank-Starling curve plots stroke volume against preload. Filling moves the heart along one curve; inotropy and heart failure shift the curve itself.
5:41Aortic stenosis vs mitral regurgitation on the pressure-volume loop
Aortic stenosis is pressure overload: a tall, narrow loop. Mitral regurgitation is volume overload: a wide loop shifted right, with no true isovolumetric sides. Read height first, then width.
5:07Fick principle: how to calculate cardiac output
The Fick principle uses oxygen as a tracer to find cardiac output from oxygen consumption and the arteriovenous oxygen content difference. Learn the formula, the sampling sites and the units trap.
5:33HFrEF vs HFpEF on the pressure-volume loop
HFrEF vs HFpEF comes down to which curve moves: a flatter ESPVR breaks emptying, a steeper EDPVR breaks filling. Both raise end-diastolic pressure and can congest the lungs.
5:15Poiseuille's law and vascular resistance: why arterioles matter
A normal pump can still produce a high pressure. Mean arterial pressure is cardiac output times resistance, and Poiseuille's law shows why arteriolar radius controls that resistance.
5:11Venous return and cardiac function curves: where they cross
Right atrial pressure is not a free input: it is set by where the cardiac function curve and the venous return curve cross. Learn which curve each change moves.
5:17The baroreceptor reflex: from stretch to vagal and sympathetic output
Stretch receptors in the carotid sinus and aortic arch report arterial pressure to the medulla, which opposes any change. Learn the arc and predict standing, bleeding and carotid massage.
4:50Myocardial oxygen supply and demand: why tachycardia causes ischaemia
Heart rate, contractility and wall tension set demand; coronary flow, mostly in diastole, sets supply. Speeding up the heart raises one and shrinks the other.
4:50Unstable angina vs NSTEMI vs STEMI: from plaque to ACS
Acute coronary syndrome starts with a clot on a disrupted plaque. How much of the artery that clot blocks decides whether you see unstable angina, NSTEMI or STEMI.
4:56Antianginal drugs: nitrates, beta blockers, calcium channel blockers
Each anti-ischaemic drug turns different dials of myocardial oxygen demand. Learn which dial each one turns, and why some of them speed the heart up.
4:59Complications of myocardial infarction, by timeline
Most post-MI complications follow what the dead wall is doing at that time. Learn the time windows and one-line signatures for arrhythmia, ruptures, aneurysm and Dressler syndrome.
What the stethoscope and the ECG show: the four heart sounds and S2 splitting, murmurs and the dynamic manoeuvres that change them, HOCM versus aortic stenosis, then the ventricular and pacemaker action potentials behind the ECG waves and intervals.
5:26S2 splitting and heart sounds S1–S4, explained
Heart sounds are valves closing. Read S2 splitting with two questions: which valve is late, and does the gap move with breathing?
5:15Heart murmurs and dynamic manoeuvres, from preload and afterload
A murmur follows the flow: manoeuvres that change preload or afterload change how much blood crosses the lesion. Hypertrophic obstructive cardiomyopathy is the exception that flips the rule.
5:31HOCM vs aortic stenosis murmur: telling them apart at the bedside
Both murmurs are harsh and systolic. The difference is the obstruction: a fixed valve in aortic stenosis, a dynamic muscle and mitral leaflet in HOCM. The manoeuvres follow from that.
5:15Ventricular action potential: phases 0 to 4 and their ion currents
A ventricular muscle cell takes about a quarter of a second to fire. Match each phase to its ion current, then to the antiarrhythmic class that acts on it.
5:17SA node pacemaker potential: phase 4 sets the heart rate
Sinoatrial nodal cells have no stable resting potential. Heart rate is the slope of phase 4, and the vagus and sympathetic nerves simply move that slope.
5:29ECG waves and intervals: what P, PR, QRS, ST and QT mean
Each ECG wave and interval maps to an electrical event in the heart. Read the gaps and you can tell where a conduction delay sits.