How to read this week
Week 2 is one organ seen from four angles: how to examine it (cardiovascular assessment), how to read its pressure (hypertension), how it fails (heart failure, staged A–D and treated by ejection fraction), and how to support it when it fails (IABP, pacemakers, AICD, ECMO). The shared theme: the ejection fraction and the blood pressure are numbers you act on, not just numbers you record.
Assessment & pressure
- The cardiac cycle, S1–S4, splits, gallops
- Murmurs — graded I through VI on Levine
- Auscultatory areas of the precordium
- ECG changes with electrolyte disturbances
- Jugular venous distension measurement
- ACC/AHA blood pressure thresholds & goals
Diagnostic currency: the stethoscope, the cuff, and the ECG.
Heart failure & device support
- HFrEF · HFmrEF · HFpEF by ejection fraction
- NYHA classes I–IV vs ACC/AHA stages A–D
- Stage C HFrEF pharmacotherapy (Table 18.3)
- ARNI, ACEI, ARB, beta-blocker, MRA, ivabradine
- IABP · pacemakers · AICD · ECMO
Diagnostic currency: ejection fraction, BNP/NT-proBNP, and echo.
Your reading map
| Ch. | Title | What it actually contains |
|---|---|---|
| 11 | Cardiovascular Assessment | Cardiac cycle · S1/S2/split S2/S3/S4 · murmurs and the Levine scale · clicks and friction rub · pulse amplitude · ECG changes with potassium/calcium/magnesium · JVD |
| 12 | Hypertension | Definition and ACC/AHA thresholds · primary vs secondary vs isolated systolic · nonpharmacologic strategy · oral and IV agents · urgency vs emergency Tables 12.1–12.6 |
| 15 | Adjunctive Therapies | IABP counterpulsation · pacemakers (types, codes, thresholds, failure modes) · AICD · ECMO (VV/VA/LAVA, indications, ACT, complications) Tables 15.1–15.4 |
| 18 | Heart Failure | Types by EF · NYHA and AHA staging · compensatory mechanisms · exam and diagnostics (BNP/NT-proBNP) · Stage C HFrEF drug doses · diuretics · ADHF Tables 18.1–18.6 |
Assessment finds the lesion. The blood pressure quantifies the load. The ejection fraction defines the failure. And when those three converge on a ventricle that can no longer keep up, the devices take over. Hold each chapter to its single question — what is it that you are measuring, and what number changes your next move?
The numbers worth carrying in
Cardiovascular Assessment
The cardiac cycle, the sounds it makes, and what an abnormal ECG and a distended neck vein tell you. Two valves close and two open in each cycle — and every murmur, gallop, and click is a report on one of those four valves or the muscle around it.
The cardiac cycle
Ventricular contraction
- AV valves close — tricuspid and mitral
- Semilunar valves open — aortic and pulmonic
Ventricular filling
- Semilunar valves close — aortic and pulmonic
- AV valves open — tricuspid and mitral
- Rapid ventricular filling — 75% of ventricular filling
- Atrial contraction (atrial kick) — the remaining 25%
The auscultatory areas
| Area | Landmark | Sound note |
|---|---|---|
| Aortic | Second right intercostal space (ICS), right sternal border, extending toward the apex | S2 louder than S1 |
| Pulmonic | Second left ICS, left sternal border | S2 louder than S1 |
| Erb's point | Third ICS, left sternal border | — |
| Tricuspid | Left lower sternal border, fifth ICS | Closure of the AV valves |
| Mitral | Fifth ICS, midclavicular line, near the cardiac apex | S1 louder than S2 |
S1 and S2
Closure of the AV valves
- Mitral and tricuspid valves close
- Occurs almost simultaneously with the apical and carotid impulses
- Coincides with the R wave on ECG
- Heard louder than S2 at the apex
Closure of the semilunar valves
- Aortic and pulmonic valves close
- Occurs at the onset of diastole (diastole lies between S2 and S1)
- Heard louder than S1 at the base of the heart
Split S2, S3, S4 — the gallops
Physiologic, on inspiration
- Late closure of the pulmonic valve + early closure of the aortic valve
- Best heard in the pulmonic area; returns to single sound in expiration
- Disappears with breath-holding; may occur every fourth heartbeat
- Normal in children and young adults
Ventricular gallop — "Ken-tuc-ky"
- Passive filling into a noncompliant left ventricle
- Early diastole, 0.12–0.16 s after S2; bell of the stethoscope at the apex
- Occurs with heart failure and cardiomyopathy when fluid overload is present
- Normal in pregnancy (hyperdynamic state of increased volume)
Atrial gallop — "Ten-ne-ssee"
- Atrial contraction into a noncompliant LV; increased ventricular diastolic pressures
- Late diastole, immediately before S1; bell at the apex
- Occurs with MI, hypertension, ventricular hypertrophy, and heart failure
- Not heard in atrial fibrillation — loss of the atrial kick
S3 and S4 heard together is a summation gallop — highly suggestive of severe myocardial failure.
Murmurs
A "blowing" or "swooshing" sound from turbulent blood flow, identified by timing, intensity, pitch, quality, location, radiation, and posture.
The Levine grading scale — how loud is it?
Murmur intensity is graded I through VI. A thrill appears at grade IV. Hover a bar for its definition.
| Pattern | Mechanism / example | Key exam finding |
|---|---|---|
| Early diastolic | Incompetent semilunar valves — aortic or pulmonic regurgitation | Decrescendo, high-pitched, heard best with the diaphragm; aortic regurgitation intensifies sitting forward with breath held |
| Diastolic rumbling | Mitral stenosis · tricuspid stenosis | Mitral stenosis: low-pitched rumble with the bell, decrescendo–crescendo, apex, better in left lateral; follows an opening snap; does not radiate |
| Midsystolic ejection | Aortic stenosis · pulmonic stenosis (obstruction of forward flow) | Aortic stenosis: harsh crescendo–decrescendo radiating to the carotids, diaphragm over the aortic area |
| Pansystolic regurgitant | Mitral regurgitation · tricuspid regurgitation (backward flow) | Mitral regurgitation: holosystolic high-pitched blowing at the apex, radiates to the left axilla; tricuspid regurgitation intensifies on inspiration |
Clicks and the friction rub
Most common click
Occurs in mid or late systole; associated with mitral valve prolapse.
Early systole
Aortic ejection click — related to stenosis, audible at apex and base. Pulmonic ejection click — audible at the base only.
Classic of pericarditis
"Scratchy," high-pitched; usually best at the apex with the patient leaning forward. Remains audible if the patient holds their breath.
ECG changes with electrolyte disturbances
Before you chase an arrhythmia, check the lytes. Filter by the ion you are tracking.
Hyperkalemia
- Tall, peaked T waves — may begin at K+ ≥ 6 mEq/L
- Widening of the QRS complex
- Prolonged P wave/PR interval — P waves flatten and widen
- Arrhythmias: bradycardia, idioventricular rhythms, VT, VFib, asystole as potassium climbs
Hypokalemia
- Changes at K+ of 3 mEq/L and below
- PVCs (unifocal and multifocal) and U waves following the T wave
- Less common: bradycardia, atrial flutter, AV block
- Potentiates digitalis toxicity
Hypercalcemia
- AV block, bundle branch block, bradycardia
- Increased contractility and shortened QT interval
- Potentiates digitalis toxicity
Hypocalcemia
- Bradycardia, ventricular ectopy, asystole — low calcium decreases contractility
- Decreased cardiac output and hypotension
- Decreased efficacy of digitalis
Hypermagnesemia
- Changes may occur with Mg > 5 mEq/L (renal failure or over-replacement)
- Prolonged PR and QT intervals, increased QRS duration
- Complete heart block and cardiac arrest at Mg > 15 mEq/L
Hypomagnesemia
- U waves, prolonged PR/QT, widened QRS, peaked then flattened T waves
- SVT, ventricular arrhythmia, torsades de pointes
- May cause hypertension and coronary/systemic vasospasm
- Must be corrected before hypokalemia/hypocalcemia replacement is effective
Jugular venous distension
How to measure central venous pressure
- Patient sitting at a 45° angle
- Assess pulsation of the internal jugular vein
- Measure in centimeters from the angle of Louis
- The angle of Louis sits ~5 cm above the right atrium
What the number means
- Add your measurement to 5 cm for the total
- 7–9 cm is normal
- Higher than 9 cm indicates volume overload
- Valves become more fibrous and rigid with calcium deposition; vessels and ventricles stiffen
- Fewer cells in the SA and AV nodes — decreased average and maximal rate
- Longer return to resting rate after stress; tachyarrhythmias are poorly tolerated because of reduced ventricular compliance
Hypertension
Sustained elevation of systolic blood pressure ≥ 120 mmHg or diastolic ≥ 80 mmHg on numerous occasions. The 2017 ACC/AHA guideline lowered the diagnosis threshold to 130/80 mmHg from the older 140/90 standard — and tied treatment to 10-year ASCVD risk, not just the cuff reading.
An average of 2 to 3 BP measurements obtained on 2 to 3 separate occasions minimizes random error. Include anyone currently taking antihypertensive agents.
The ACC/AHA categories
< 120 / < 80 mmHg
Both systolic and diastolic below threshold. Promote optimal lifestyle habits; reassess in one year.
120–129 / < 80 mmHg
Nonpharmacologic therapy; reassess in 3–6 months.
130–139 or 80–89 mmHg
Nonpharmacologic therapy. Add medication if clinical ASCVD or estimated 10-year risk ≥ 10% — then reassess in one month; otherwise reassess in 3–6 months.
≥ 140 or ≥ 90 mmHg
Nonpharmacologic therapy plus BP-lowering medication; consider two agents of different classes. Reassess in one month.
The blood pressure thresholds, on one scale
Systolic readings run left to right. When SBP and DBP fall in different categories, assign the higher one. Hover a zone.
Three ways hypertension presents
Essential / idiopathic — 95%
- Cause unknown; onset usually ages 25–55
- Exacerbating: obesity, alcohol > 2 drinks/day, smoking, NSAID use
- Theories: genetics/environment, elevated intracellular calcium & sodium, sympathetic hyperactivity, high renin–angiotensin activity
Known cause — 5%
- Estrogen (oral contraceptives, hormone replacement)
- Renal disease
- Pregnancy
- Endocrine disorders — e.g., pheochromocytoma
Most common in the elderly
- SBP > 140 mmHg with DBP < 90 mmHg
- May account for 65%–75% of HTN in the elderly
- Dihydropyridine CCBs and thiazides preferred first-line; avoid beta-blockers
Who starts medication, and at what threshold
| Population | Threshold (mmHg) | Goal (mmHg) |
|---|---|---|
| Clinical CVD or 10-year ASCVD risk ≥ 10% | ≥ 130/80 | < 130/80 |
| No clinical CVD and 10-year ASCVD risk < 10% | ≥ 140/90 | < 130/80 |
| Older persons (≥ 65; noninstitutionalized, ambulatory, community-living) | ≥ 130 (SBP) | < 130 (SBP) |
| Diabetes mellitus | ≥ 130/80 | < 130/80 |
| Chronic kidney disease (incl. after transplant) | ≥ 130/80 | < 130/80 |
| Heart failure | ≥ 130/80 | < 130/80 |
| Stable ischemic heart disease | ≥ 130/80 | < 130/80 |
| Secondary stroke prevention (lacunar) | ≥ 130/80 | < 130/80 |
| Secondary stroke prevention | ≥ 140/90 | < 130/80 |
| Peripheral arterial disease | ≥ 130/80 | < 130/80 |
- Sodium restriction — initial ≤ 100 mmol/day (2.4 g sodium or 6 g salt); optimal < 1500 mg/day, but aim for at least a 1000 mg/day reduction
- Weight loss if overweight
- DASH diet — fruits, vegetables, low-fat dairy; reduced saturated and total fat
- Aerobic exercise 30–45 min/day on most days
- Alcohol — fewer than 2 drinks/day (men) or 1 (women and lighter-weight persons)
- Smoking cessation
- Adequate potassium, calcium, and magnesium intake
Pharmacologic measures
First-line agents are thiazide diuretics, CCBs, and ACEIs or ARBs. Beta-blockers are second-line unless there is a compelling indication (post-MI, CAD, HF).
| Class | Representative doses | Cautions |
|---|---|---|
| Thiazide diuretics | Chlorthalidone 12.5–25 mg daily · HCTZ 25–50 mg daily · Indapamide 1.25–2.5 mg daily · Metolazone 2.5–5 mg daily | Chlorthalidone preferred (long half-life, proven CVD reduction). Monitor hyponatremia, hypokalemia, uric acid, calcium. Generally avoided when eGFR < 30 mL/min. |
| ACEIs | Lisinopril 10–40 mg daily · Enalapril 5–40 mg daily or BID · Ramipril 2.5–20 mg daily | Do not use with ARBs or a direct renin inhibitor. Do not initiate if K+ > 5.5 mEq/L. Contraindicated in pregnancy, bilateral renal artery stenosis. May cause cough, angioedema. |
| ARBs | Losartan 50–100 mg daily · Valsartan 80–320 mg daily or BID · Candesartan 8–32 mg daily | Reserved for ACEI-intolerant patients. Same hyperkalemia/pregnancy/renal-artery cautions; less cough than ACEIs. |
| CCBs — dihydropyridine | Amlodipine 2.5–10 mg daily · Nifedipine 30–90 mg daily | Peripheral vasodilation; dose-related pedal edema (more common in women). Amlodipine/felodipine usable in HFrEF if needed for BP. |
| CCBs — nondihydropyridine | Diltiazem ER 120–480 mg daily · Verapamil ER 100–480 mg daily | Do not use in HFrEF. Avoid routine use with beta-blockers (bradycardia/heart block). |
| Beta-blockers | Metoprolol succinate 50–200 mg daily · Carvedilol 12.5–50 mg BID · Atenolol 25–100 mg daily | Not first-line unless ischemic heart disease or HF. Caution in asthma/COPD (bronchospasm). Avoid abrupt cessation. |
| Aldosterone antagonists | Spironolactone 25–100 mg daily · Eplerenone 50–100 mg daily or BID | Preferred in primary aldosteronism and resistant HTN. Avoid with K+ supplements or significant renal dysfunction. Spironolactone — greater gynecomastia/impotence risk. |
Urgency vs. emergency
Severe BP, no organ damage
Severe BP elevation in an otherwise stable patient without acute or impending target organ damage — often noncompliance or withdrawal from therapy. Treated by reinstituting or intensifying oral therapy; parenteral therapy is rarely required.
Oral options: Captopril 12.5–25 mg PO · Clonidine 0.2 mg PO then 0.1 mg hourly to a total of 0.8 mg · Labetalol 100–400 mg PO (off-label).
> 180/120 with organ damage
Severe elevation (> 180/120 mmHg) with new or worsening target organ damage — encephalopathy, intracerebral hemorrhage, acute ischemic stroke, acute MI, acute LV failure with pulmonary edema, dissecting aortic aneurysm, acute renal failure, eclampsia.
Requires immediate reduction (not necessarily to normal) to limit further damage.
Lower BP to 160–180 mmHg systolic or < 105 mmHg diastolic — no more than 25% within minutes to 1–2 hours — then gradually lower over several days with oral therapy to prevent coronary, cerebral, or renal ischemia. No single agent is proven superior; choose by target organ, pharmacokinetics, and the medication's hemodynamic/adverse-effect profile.
Heart Failure
A clinical syndrome, not a single disease — the heart cannot pump or fill well enough to meet tissue demands. Everything in this chapter hangs on one number: the ejection fraction.
Three types, one number
Ejection fraction defines the type of failure
HFrEF is systolic failure; HFpEF is a filling problem with a normal EF. Hover a zone.
Systolic failure
- Impaired contractility → reduced stroke volume and cardiac output
- Associated with eccentric hypertrophy
Preserved EF
- Nondilated LV with elevated LV filling pressures
- Normal contractility but impaired ventricular filling (relaxation)
- Concentric hypertrophy; cardiothoracic ratio < 55% on AP chest film
Two classification systems
Classified by symptoms
- Class I — no limitation of activity
- Class II — slight limitation; comfortable at rest or with mild exertion
- Class III — marked limitation; comfortable only at rest
- Class IV — complete rest; any activity brings discomfort, symptoms at rest
Classified by structure and progression
- Stage A — high risk, no structural disease
- Stage B — structural disease, no symptoms
- Stage C — structural disease with symptoms
- Stage D — refractory HF
High risk, no structural disease
- Hypertension, CAD, diabetes, obesity, metabolic syndrome — or cardiotoxin use / family history of cardiomyopathy
- Goal: heart-healthy lifestyle, prevent vascular/coronary disease and LV structural abnormalities
- Drugs: ACEI/ARB in appropriate patients; statins as appropriate
Structural disease, no symptoms
- Previous MI; LV remodeling (LVH, low EF); asymptomatic valvular disease
- Goal: prevent HF symptoms and further remodeling
- Drugs: ACEI/ARB and beta-blockers as appropriate; ICD in selected patients
Structural disease with symptoms
- Known structural disease plus HF signs and symptoms
- Goal: control symptoms, improve quality of life, prevent hospitalization and mortality
- Routine drugs: diuretics for fluid retention, ACEI/ARB, ARNI, beta-blockers, aldosterone antagonists
Refractory HF
- Marked symptoms at rest; recurrent hospitalizations despite guideline-directed medical therapy (GDMT)
- Options: heart transplant, chronic inotropes, temporary/permanent mechanical circulatory support, palliative care and hospice, ICD deactivation
Stages A through D — the progression
Each step adds structure, then symptoms, then refractoriness. Hover a stage for its definition.
Predisposing and precipitating factors
Coronary artery disease
LV dysfunction from CAD is the most common cause of chronic HF. MI with atherosclerotic CVD carries an 8–10× increased risk of subsequent HF from ventricular remodeling.
Hypertension
Risk is 3× higher in patients with HTN — the leading risk factor for acute HF.
Everything that adds load
- Diabetes mellitus; metabolic syndrome
- Physical inactivity, obesity, smoking
- Excessive alcohol intake
- Infections, thyroid disease, pregnancy, cardiomyopathy, valvular disease
- Hypertrophy — wall thickens with increased muscle mass; higher myocardial oxygen demand.
- Dilatation — chambers enlarge; stretched fibers increase contractile force (Frank-Starling) up to a point, then overstretching impairs actin–myosin interaction and contractile force falls.
- Sympathetic nervous system — inadequate CO releases epinephrine/norepinephrine → increased heart rate, increased SVR (afterload), increased myocardial oxygen demand.
- Renal (RAAS) — decreased CO → renin → angiotensin I → angiotensin II (via ACE) → vasoconstriction + aldosterone → sodium retention → ADH → water retention.
Physical exam — left vs. right
Into the lungs
- Rales; crackles and wheezes; dyspnea
- Bilateral infiltrates on chest radiograph
- S3 (ventricular gallop) common; rarely S4
- Atrial fibrillation (atrial distention)
- Pulsus alternans — every other pulse beat diminished
- Increased pulmonary capillary wedge pressure; pulmonary edema
Into the systemic veins
- Increased central venous pressure; JVD
- Peripheral edema
- Hepatomegaly with hepatojugular reflux
- Ascites
- S3 and/or S4 heart sounds
Symptoms and diagnostics
What the patient reports
- Fatigue — may be an early sign; dyspnea
- Orthopnea; paroxysmal nocturnal dyspnea or nocturnal cough (usually 1–3 hr after falling asleep)
- Cough; tachycardia; edema (legs, liver, spleen, abdomen, lungs)
- Nocturia — supine fluid shifts back into the intravascular space
- Weight gain of 1 kg = 1 L of fluid
BNP and the rest
- BNP indicates ventricular dysfunction; mean by age: 55–64 → 26 pg/mL; 65–74 → 31 pg/mL; ≥ 75 → 63 pg/mL
- NT-proBNP — < 125 pg/mL under age 75; < 450 pg/mL at 75+ (rises with age and renal dysfunction)
- Electrolytes, BUN/creatinine/GFR, glucose, lipids, LFTs, TSH
- ECG, chest radiograph (cardiomegaly/congestion), echocardiogram (EF, valves, wall motion)
HFrEF — ACEI (or ARB/ARNI), beta-blocker, aldosterone antagonist, diuretic for congestion. HFpEF — control BP to systolic < 130 mmHg, sodium restriction, diuretic for fluid overload, MRA, beta-blocker if prior MI/HTN/atrial fibrillation. ADHF — IV loop diuretics first, continue the beta-blocker, add vasodilators (nitroglycerin/nitroprusside) if not hypotensive, reserve inotropes (milrinone/dobutamine) for hypotension with poor perfusion. The dose tables live in the next section.
Heart Failure Pharmacotherapy
The Stage C HFrEF drug ladder, reproduced from Table 18.3. Every dose below is the initial → maximum path a prescriber walks; the mean doses achieved in clinical trials show how far real patients actually get. Filter by class.
- ARNI (sacubitril/valsartan) cannot be used with an ACEI/ARB, or within 36 hours of an ACEI dose — and is off the table with a history of angioedema.
- Aldosterone antagonists require creatinine ≤ 2.5 mg/dL (men) or ≤ 2.0 (women), or eGFR > 30 mL/min/1.73 m², and potassium < 5.0 mEq/L.
- Ivabradine is added when the patient is in sinus rhythm on maximum tolerated beta-blocker with HR > 70 — or when they cannot tolerate a beta-blocker.
ACE inhibitors — first-line
- Captopril 6.25 mg TID → 50 mg TID mean 122.7 mg/day
- Enalapril 2.5 mg BID → 10–20 mg BID mean 16.6 mg/day
- Lisinopril 2.5–5 mg daily → 20–40 mg daily mean 32.5–35 mg/day
- Ramipril 1.25–2.5 mg daily → 10 mg daily
- Fosinopril 5–10 mg → 40 mg daily · Perindopril 2 mg → 8–16 mg · Quinapril 5 mg → 20 mg · Trandolapril 1 mg → 4 mg
Angiotensin receptor blockers
- Candesartan 4–8 mg daily → 32 mg daily mean 24 mg/day
- Losartan 25–50 mg daily → 50–150 mg daily mean 129 mg/day
- Valsartan 20–40 mg BID → 160 mg BID mean 254 mg/day
For patients who cannot tolerate an ACEI (cough or angioedema).
Sacubitril / valsartan
- 49/51 mg BID → 97/103 mg BID may start at 24/26 mg BID; target 24/26, 49/51, or 97/103 mg BID
Replaces an ACEI/ARB in NYHA II–III HFrEF who tolerate it. Not with an ACEI/ARB or within 36 hr of an ACEI dose; not with angioedema history.
Beta-blockers
- Carvedilol 3.125 mg BID → 50 mg BID mean 37 mg/day
- Bisoprolol 1.25 mg daily → 10 mg daily mean 8.6 mg/day
- Metoprolol succinate ER 12.5–25 mg daily → 200 mg daily mean 159 mg/day
- Carvedilol CR 10 mg daily → 80 mg daily
Recommended for all HFrEF — even with DM, COPD, or PVD. Caution with recurrent hypoglycemia, asthma, or resting limb ischemia.
Aldosterone (mineralocorticoid) antagonists
- Spironolactone 12.5–25 mg daily → 25 mg daily or BID mean 26 mg/day
- Eplerenone 25 mg daily → 50 mg daily mean 42.6 mg/day
NYHA II–IV HFrEF to reduce morbidity/mortality. Requires K+ < 5.0 and adequate renal function (creatinine ≤ 2.5 men / ≤ 2.0 women, or eGFR > 30).
Ivabradine
- 5 mg daily → 7.5 mg daily mean 6.4 mg BID at 28 days; 6.5 mg BID at 1 year
Inhibits the If current in the SA node. Add for sinus rhythm with HR > 70 on GDMT, or beta-blocker intolerance.
Isosorbide dinitrate + hydralazine
- Fixed-dose combo 20 mg / 37.5 mg TID → 40 mg / 75 mg TID mean ~90/175 mg daily
- Separate 20–30 mg isosorbide + 25–50 mg hydralazine TID → 40 mg isosorbide TID + 100 mg hydralazine TID
Standard add-on for African Americans with NYHA III–IV HFrEF (in addition to beta-blocker + ACEI).
Two dose ladders worth memorizing
Carvedilol and sacubitril/valsartan — the two most distinctive titrations in the table. Hover a step.
Digoxin and the diuretics
Narrow therapeutic range
- 0.125 mg daily in most patients (by lean body mass, renal function, and other drugs)
- Goal level 0.5–0.9 ng/mL; high doses (> 0.25 mg daily) not recommended for rate control
- Monitor digoxin and potassium closely — toxicity can occur even at "normal" levels, especially with hypokalemia
Class of choice in HF
- Restore and maintain normal volume; loop, not thiazide, is usually necessary
- After initial short-acting therapy, more frequent dosing (BID–TID) beats larger single doses
- Oral torsemide for poor absorption or erratic effect — especially right-sided HF with refractory retention
| Drug | Initial daily dose | Max daily | Duration of action |
|---|---|---|---|
| Bumetanide | 0.5–1 mg once or twice | 10 mg | 4–6 hr |
| Furosemide | 20–40 mg once or twice | 600 mg | 6–8 hr |
| Torsemide | 10–20 mg once | 200 mg | 12–16 hr |
| Chlorothiazide | 250–500 mg once or twice | 1,000 mg | 6–12 hr |
| Chlorthalidone | 12.5–25 mg once | 100 mg | 24–72 hr |
| Hydrochlorothiazide | 25 mg once or twice | 200 mg | 6–12 hr |
| Indapamide | 2.5 mg once | 5 mg | 36 hr |
| Metolazone | 2.5 mg once | 20 mg | 12–24 hr |
| Spironolactone | 12.5–25 mg once | 50 mg | 1–3 hr |
| Amiloride | 5 mg once | 20 mg | 24 hr |
| Triamterene | 50–75 mg twice | 200 mg | 7–9 hr |
Sequential nephron blockade: add metolazone 2.5–10 mg once, or HCTZ 25–100 mg once/twice, or IV chlorothiazide 500–1,000 mg once to a loop diuretic for persistent retention — but avoid long-term daily use (especially metolazone) because of electrolyte shifts and volume disturbance.
- Impaired renal function is a risk factor; risk rises progressively when serum creatinine > 1.6 mg/dL. Confirm eGFR/creatinine clearance > 30 mL/min/1.73 m² when creatinine is unreliable.
- Do not ordinarily initiate if baseline potassium > 5.0 mEq/L.
- Typical start: spironolactone 12.5 mg or eplerenone 25 mg, then up to 25 mg or 50 mg if appropriate.
- Higher ACEI doses raise risk (captopril ≥ 75 mg/day; enalapril or lisinopril ≥ 10 mg/day).
- Discontinue or reduce potassium supplements when starting.
- Check potassium and renal function at 3 days and 1 week, then at least monthly for the first 3 months.
Mechanical & Device Support
When the pump cannot keep up, four tools take over the job: the intra-aortic balloon pump (counterpulsation), the pacemaker (rhythm), the AICD (lethal arrhythmia), and ECMO (rest for the heart and/or lungs). Filter to the device you need.
Intra-aortic balloon pump
- Inflates during diastole (aortic valve closed) → displaces blood backward (coronary perfusion) and forward (vital organs)
- Deflates just before systole → reduces aortic pressure, afterload, and myocardial demand
- Goal: increase coronary perfusion and decrease O₂ consumption
Pacemakers
- Deliver electrical stimuli to keep adequate heart rate and cardiac output
- Modes: AAI, VVI, DDD (chamber paced → chamber sensed → response)
- Types: transcutaneous, transvenous (most common permanent), leadless, epicardial
Automatic internal cardioverter/defibrillator
- Automatically treats ventricular tachycardia and ventricular fibrillation
- Primary prevention: EF < 35% (ischemic or nonischemic, no acute reversible cause)
- Types: single-, dual-chamber, CRT, wearable LifeVest
Extracorporeal membrane oxygenation
- Rests the lungs and/or heart in reversible respiratory and/or cardiac failure
- VV-ECMO — respiratory support; VA-ECMO — cardiac support
- ACT goal typically 180–210
IABP — the balloon pump
When to consider it
- Acute myocardial infarction; cardiogenic shock
- Preinfarction angina refractory to drugs
- Refractory ventricular arrhythmias related to ischemia
- Severe mitral regurgitation; severe ventriculoseptal defect
- Low cardiac output states; after heart surgery
When it is off the table
- Aortic aneurysm and/or dissection
- Bypass grafting from the aorta to peripheral vessels
- Aortic insufficiency / regurgitation
Relative: peripheral/central atherosclerosis, prior embolic event, severe PVD, hepatic disease/coagulopathy, and ethical considerations (advanced age, severe LV failure, multisystem failure, metastatic cancer).
Timing checklist (optimal inflation/deflation)
- Inflated at the dicrotic notch (DN); clear "V" at the inflation point
- Peak diastolic pressure (PDP) ≥ peak systolic pressure (PSP)
- Balloon aortic end-diastolic pressure (BAEDP) is 5–15 mmHg less than the patient's aortic end-diastolic pressure (PAEDP)
- Assisted peak pressure < PSP; end-diastolic dip = BAEDP − PAEDP = 5–15 mmHg
Management
- Keep the involved leg straight; head of bed elevated only slightly (≤ 30°)
- Monitor for lower-extremity ischemia, catheter displacement (dampened/flattened waveform), balloon perforation (blood in gas circuit), infection
Weaning parameters
- Cardiac index 2.5 L/min or >; MAP > 70 mmHg; pulmonary capillary wedge pressure 6–12 mmHg; no chest pain; no signs of inadequate perfusion
- Method: decrease balloon volume (e.g., 25% reductions) or decrease inflation frequency (every other, then every third beat)
Pacemakers
The stimulus depolarizes
Delivered impulse adequate to depolarize cardiac muscle — a paced P wave (atrial) or QRS (ventricular) follows each pacing spike.
The pacemaker recognizes
Recognizes intrinsic activity and resets its timer, inhibiting the stimulus to prevent competition with the intrinsic pacemaker.
Rate, output, sensitivity
Rate (fires/min) · energy output (mA, set 2–3× threshold) · sensitivity (mV; lower number = more sensitive, e.g. 2–3 mV).
| Type | What it is | Note |
|---|---|---|
| Transcutaneous | External, anterior + posterior pads; ventricular pacing in emergencies (e.g., severe bradycardia) | Temporary; painful — sedate |
| Transvenous | Pulse generator under skin (upper chest); lead via subclavian vein into RA/RV | Most common permanent type |
| Leadless | All-in-one capsule, no leads; RV apex via femoral vein | Introduced 2016; ventricular pacing only |
| Epicardial | Leads sewn to epicardium after cardiac surgery; exit the chest | Discontinued 1–3 days post-op |
The five-position code — chamber paced · chamber sensed · mode of response · programmable functions · tachyarrhythmia functions. The first three letters are used most: AAI (atrial pace/sense/inhibited) · VVI (ventricular) · DDD (dual).
| Failure | How it looks | What to do |
|---|---|---|
| Failure to capture | Pacing artifact with no complex following the spike | Position left side; check CXR; increase amplitude/mA; change battery (temporary) or generator (permanent) |
| Failure to pace (fire) | Absent artifact when firing should have occurred | Position left side; check CXR; remove EMI sources (MRI, radio towers); warm if shivering; decrease sensitivity (increase mV); change battery/generator |
| Failure to sense (undersensing) | Random spikes competing with intrinsic rhythm | Position left side; check CXR; enhance sensitivity (decrease mV); use magnet briefly; turn off if cardiac output stable |
AICD
EF < 35%
- Patients who have not had VFib/VT but are at increased risk — EF < 35%, ischemic or nonischemic, no acute reversible cause
- CRT-P: AV block with EF 35–50% · CRT-D: LBBB with EF ≤ 35%
- CRT indicated in symptomatic HF with LBBB, wide QRS, severe LV dysfunction
Survived VT / VFib
- Survivors of an episode of VT or VFib
- Programmable therapies: defibrillation (unsynchronized, VFib) · cardioversion (synchronized, AFib/VT) · antitachycardia pacing (ATP) · antibradycardia pacing (ABP)
- Over 1 million people worldwide have AICDs
- Document device-related events; maintain MedicAlert identification
- Train family/significant others in CPR
- Magnets may activate or deactivate the device — monitor for tones signaling deactivation after magnet exposure
ECMO
Respiratory support
- Blood drained from right internal jugular/SVC, oxygenated, returned to the right atrium
- Indications: ARDS, pneumonia, pulmonary contusion, asthma, drowning, smoke inhalation, airway obstruction, bridge to transplant
- Venous cannulas typically 20–27 Fr
Cardiac support
- Blood removed from the right atrium, returned to the arterial circulation
- Indications: massive PE, refractory cardiogenic shock, cardiac arrest (eCPR), myocarditis, acute MI, sepsis, bridge to transplant/VAD
- Aortic cannulas typically 15–19 Fr; distal reperfusion catheter to protect the limb
VV-ECMO severity
- 50% mortality: PaO₂ < 150 on > 90% FiO₂ (Murray 2–3)
- 80% mortality: PaO₂ < 80 on FiO₂ > 90% (Murray 3–4)
Weigh carefully
- Heparin allergy / anticoagulation issues
- Refusal of blood products; morbid obesity; elderly
- Major peripheral vascular disease (VA-ECMO)
Do not start
- Irreversible cardiac dysfunction (not a transplant/VAD candidate)
- Unwitnessed arrest or CPR > 60 min; widespread malignancy
- Severe neurologic dysfunction; aortic dissection; severe aortic regurgitation
Management
- Monitor pump speed/flow, circuit and blood gases; ACT goal 180–210 (or anti-Xa/PTT per institution)
- After cannulation: CXR and echocardiogram; right radial arterial line; Doppler pulses (radial, dorsalis pedis/posterior tibial); distal limb perfusion in femoral access
- Anticoagulation: heparin bolus then drip once ACT < 200; bivalirudin for HIT
On VA support — no chest compressions
- VA-ECMO is already perfusing/oxygenating; consider cardioversion or chemical code, or increase to full flow
- Major VA complications: LV distention/thrombus, Harlequin (North-South) syndrome, lower-extremity ischemia, hemorrhage
Chatter (venous access insufficiency)
- Sucking down on the inlet cannula, bouncing tubing, hypovolemia, cannula position
- Intervention: find bleeding, adjust flows down then slowly up, give volume, check for kinks/clots, inspect cannula position
Weaning (VA)
- Add inotropes (dobutamine/milrinone) and vasopressors (epinephrine); decrease RPMs or flow in increments to "idle" — no less than 2 L/min
IABP augments a beating heart (counterpulsation, lower afterload, more coronary flow). ECMO replaces the failing organ's job — VV for the lungs, VA for the heart and lungs — while reversible failure recovers. IABP needs its own pulse; ECMO does not.
What to lock in
If this week supports one study habit, it is anchoring every concept to its decisive number or first move. These are the high-yield contrasts to carry forward.
S1 vs. S2
S1 = AV valves (mitral/tricuspid) close, loudest at the apex. S2 = semilunar valves (aortic/pulmonic) close, loudest at the base.
S3 vs. S4 gallops
S3 = "Ken-tuc-ky," early diastole, normal in pregnancy. S4 = "Ten-ne-ssee," late diastole before S1, lost in atrial fibrillation.
HFrEF vs. HFpEF
HFrEF ≤ 40% — systolic failure. HFpEF ≥ 50% — preserved EF with elevated filling pressures. HFmrEF 41–49% — treated like HFpEF.
Urgency vs. emergency
Both are severe BP — but emergency = > 180/120 with new/worsening target organ damage. Urgency has no organ damage and rarely needs parenteral therapy.
Stage C HFrEF ladder
ACEI (or ARB) + beta-blocker → replace with ARNI if tolerated → add aldosterone antagonist → add ivabradine (HR > 70) or hydralazine/nitrate (African American, NYHA III–IV). Diuretic for congestion.
ADHF first moves
IV loop diuretic first → continue the beta-blocker → add vasodilator (nitroglycerin/nitroprusside) if not hypotensive → reserve inotropes (milrinone/dobutamine) for hypotension with poor perfusion.
Pacemaker failure
Left side first, then CXR, then reprogram. Capture → raise mA; pace → decrease sensitivity (raise mV); sense → decrease mV. Change battery or generator as needed.
The 130/80 threshold
2017 ACC/AHA lowered the HTN diagnosis to 130/80 mmHg (from 140/90). High ASCVD risk starts medication at ≥ 130/80; lower risk waits for ≥ 140/90.
IABP timing
Inflate in diastole, deflate just before systole. It raises coronary perfusion and lowers afterload and myocardial oxygen demand.
Primary-prevention ICD
EF < 35%, ischemic or nonischemic, with no acute reversible cause. CRT-D for LBBB with EF ≤ 35%.
ECMO numbers
ACT 180–210. VV-ECMO = lungs; VA-ECMO = heart (returns to arterial circulation). No chest compressions on VA.
Digoxin in HF
0.125 mg daily, goal level 0.5–0.9 ng/mL. Narrow therapeutic range; monitor digoxin and potassium closely.
Listen for the valve, measure the pressure, define the failure by its ejection fraction, treat the failure by its stage — and let the machine take over only when the muscle cannot.
Rapid-fire review
Answer out loud first, then reveal. Fifteen questions covering all four chapters.
During systole, which valves close and which open?
AV valves (tricuspid and mitral) close; semilunar valves (aortic and pulmonic) open. In diastole the semilunar valves close and the AV valves open, with rapid ventricular filling (75%) and the atrial kick (25%).
Where is the mitral area auscultated, and which heart sound is louder there?
Fifth intercostal space, midclavicular line, near the cardiac apex — S1 is louder than S2 at the apex (the reverse is true at the aortic and pulmonic areas at the base).
Which gallop sounds like "Ken-tuc-ky," when does it occur, and in what normal state is it heard?
S3 (ventricular gallop), early in diastole (0.12–0.16 s after S2), from passive filling of a noncompliant left ventricle. It occurs in heart failure and cardiomyopathy with fluid overload — and is normal in pregnancy (hyperdynamic state of increased volume).
Which heart sound is not heard in atrial fibrillation, and why?
S4 (atrial or presystolic gallop) — it is produced by atrial contraction, so it disappears with the loss of the atrial kick in atrial fibrillation.
A murmur is very loud, heard with one corner of the stethoscope off the chest wall, and there is a palpable thrill. What Levine grade is it?
Grade V/VI. (Grade IV is loud with a thrill; grade VI is loudest, audible without a stethoscope, still with a thrill.)
A "scratchy," high-pitched sound that remains audible when the patient holds their breath suggests what?
A pericardial friction rub — the classic sound of pericarditis. It is usually heard best at the apex with the patient leaning forward.
State the four ACC/AHA blood pressure categories with their systolic/diastolic values.
Normal < 120 / < 80 · Elevated 120–129 / < 80 · Stage 1 130–139 or 80–89 · Stage 2 ≥ 140 or ≥ 90. If SBP and DBP fall in different categories, assign the higher one.
What proportion of hypertension is primary (essential), and at what ages does it usually onset?
95% is primary/essential/idiopathic, with onset usually between ages 25 and 55. Secondary causes account for only 5%.
Define a hypertensive emergency and state the target for the first reduction of blood pressure.
Severe elevation (> 180/120 mmHg) with new or worsening target organ damage. Lower to 160–180 mmHg systolic or < 105 mmHg diastolic — no more than 25% within minutes to 1–2 hours — then gradually over several days.
What ejection fraction values define HFrEF, HFmrEF, and HFpEF?
HFrEF ≤ 40% (systolic failure) · HFmrEF 41–49% (treated like HFpEF) · HFpEF ≥ 50% (preserved EF with elevated filling pressures).
A Stage C HFrEF patient (NYHA II) tolerates an ACE inhibitor. What replacement is recommended, and what is the washout rule?
An ARNI (sacubitril/valsartan) — the ACE inhibitor must be stopped 36 hours before starting the ARNI, which cannot be used with an ACEI/ARB and should not be given with a history of angioedema.
Give carvedilol's starting and maximum doses in heart failure.
Start 3.125 mg BID, titrate up to 50 mg BID (mean achieved in trials ≈ 37 mg/day).
When is ivabradine added in HFrEF, and what is its mechanism?
For symptomatic NYHA II–III HFrEF on GDMT, in sinus rhythm with HR > 70 despite maximum tolerated beta-blocker — or when the patient cannot tolerate a beta-blocker. It inhibits the If current in the SA node.
The IABP inflates and deflates at what points of the cardiac cycle?
Inflates during diastole (aortic valve closed) to raise coronary and vital-organ perfusion, and deflates just before systole to reduce afterload and myocardial oxygen demand.
What ejection fraction qualifies a patient for a primary-prevention ICD, and what is the typical ECMO ACT goal?
Primary-prevention ICD: EF < 35% (ischemic or nonischemic, no acute reversible cause). ECMO anticoagulation: ACT 180–210 (or anti-Xa/PTT per institution).
Sources
Every statement above comes from the assigned Week 2 reading — four chapters of Practice Considerations for Adult-Gerontology Acute Care Nurse Practitioners.
Chapters
King, J. (2021). Cardiovascular assessment. In Practice considerations for adult-gerontology acute care nurse practitioners (3rd ed., Chapter 11).
Vandewaa, E., & Fellin, R. (2021). Hypertension. In Practice considerations for adult-gerontology acute care nurse practitioners (3rd ed., Chapter 12).
Melander, S. D., & Bauman, J. (2021). Adjunctive therapies. In Practice considerations for adult-gerontology acute care nurse practitioners (3rd ed., Chapter 15).
King, J. (2021). Heart failure. In Practice considerations for adult-gerontology acute care nurse practitioners (3rd ed., Chapter 18).
Selected sources cited in the reading
Whelton, P. K., Carey, R. M., Aronow, W. S., Casey, D. E., Jr., Collins, K. J., Himmelfarb, C. D., . . . Wright, J. T., Jr. (2017). ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA guideline for the prevention, detection, evaluation, and management of high blood pressure in adults. Hypertension, 71(6), e13–e115.
Yancy, C. W., Jessup, M., Bozkurt, B., Butler, J., Casey, D. E., Jr., Drazner, M. H., . . . American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. (2013). 2013 ACCF/AHA guideline for the management of heart failure. Circulation, 128(16), e240–e327.
Yancy, C. W., Jessup, M., Bozkurt, B., Butler, J., Casey, D. E., Jr., Colvin, M. M., . . . Westlake, C. (2017). 2017 ACC/AHA/HFSA focused update of the 2013 ACCF/AHA guideline for the management of heart failure. Journal of the American College of Cardiology, 70(6), 776–803.
Krishna, M., & Zacharowski, K. (2009). Principles of intra-aortic balloon pump counterpulsation. Continuing Education in Anesthesia, Critical Care, & Pain, 9(1), 24–28.
Patterson, T., Perera, D., & Redwood, S. R. (2014). Intra-aortic balloon pump for high-risk percutaneous coronary intervention. Circulation: Cardiovascular Interventions, 7(5), 712–720.
Ball, J. W., Dains, J. E., Flynn, J. A., Solomon, B. S., & Stewart, R. W. (2015). Seidel's guide to physical examination (8th ed.). St. Louis, MO: Mosby Elsevier.